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Copyright of Chinese Journal of Contemporary Pediatrics is the property of Xiangya Medical Periodical Press and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

To explored the protective effect and mechanism of Chinese yam total protein in human umbilical vein endothelial cells (HUVECs) with high-concentration D-glucose (HG)-induced oxidative stress injury. The HUVECs injury model was established by 50 mmol/L HG. HUVECs were randomly divided into control, model, low-dose Chinese yam total protein (0.5 mg/mL), and high-dose Chinese yam total protein (1 mg/mL) groups. The effects of Chinese yam total protein on the viability, morphology, and angiogenetic ability of HUVECs treated with HG were evaluated. The reactive oxygen species (ROS) level, superoxide dismutase (SOD) and catalase (CAT) activities in cells were determined. The nitric oxide (NO), 8-hydroxy deoxyguanosine (8-OHdG), malondialdehyde (MDA), interleukin-1β (IL-1β), and interleukin-6 (IL-6) levels in culture medium supernatant were measured. Protein expression levels of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X (Bax), thioredoxin-interacting protein (Txnip), NOD-like receptor protein 3 (NLRP3), cleaved Caspase-1, and IL-1β were determined. The results showed that Chinese yam total protein could significantly increased the cell viability of HUVECs treated with HG (P<0.01), improved cell apoptotic morphology, and significantly increased the activities of SOD and CAT (P<0.05, P<0.01) and ratio of apoptosis-related proteins (Bcl-2/Bax), angiogenetic ability and nitric oxide (NO) secretion. Moreover, Chinese yam total protein significantly decreased the levels of ROS, MDA, 8-OHdG, IL-1β, and IL-6 (P<0.05, P<0.01) and the expression levels of inflammation-related proteins (Txnip, NLRP3, cleaved Caspase-1, and IL-1β) (P<0.05, P<0.01). Changes in these indicators showed a significant concentration-dependent manner. The results indicate that Chinese yam total protein may protect against HG-induced oxidative stress by inhibiting the Txnip/NLRP3 signaling pathway, restoring the oxidative balance, and reducing the inflammatory response of HUVECs. [ABSTRACT FROM AUTHOR]

Objective: To explore the effects of kinesin-13 family member 2C (KIF2C) on hepatocellular carcinoma (HCC) cell proliferation, invasion and migration as well as human umbilical vein endothelial cell (HUVEC) angiogenesis to provide potential targets for HCC treatment. Methods: Database data were used to analyze the expression of KIF2C mRNA and protein in HCC tissues and its correlation with the expression of angiogenesis-associated factors (VEGFR2 and HIF-1α). Human normal hepatocytes QSG-7701, HUVEC, and HCC cells Huh-7 and Hep3B2.1-7 were routinely cultured, and sh-NC and sh KIF2C were transfected into Huh-7 and Hep3B2.1-7 cells with Lipofectamine 3000 transfection reagent. qPCR was performed to detect the expression of KIF2C mRNA in QSG-7701, Huh-7 and Hep3B2.1-7 cells of each group, and WB was performed to detect the expression of KIF2C protein in cells of each group, and the effect of KIF2C knockdown on the clone formation of Huh3B2.1-7 and Huh-7 cells was examined in the clonogenic assay. Tubulogenesis assay to detect the effect of conditioned cultures of knockdown KIF2C-expressing Huh-7 and Hep3B2.1-7 cells on the angiogenic capacity of HUVEC cells. Results: Database analysis showed that KIF2C mRNA and protein were highly expressed in HCC tissues (both P<0.01). In addition, database analysis suggested that KIF2C mRNA may also be highly expressed in HCC cells, and the results of KIF2C mRNA and protein expression detected by qPCR and WB showed that its mRNA and protein were highly expressed in HCC cells (both P<0.01), consistent with the database data analysis. Database data analysis also showed that KIF2C was positively correlated with the expression levels of VEGFR2 and HIF-1α in HCC tissues (P<0.05 or P<0.01). Stable low KIF2C-expressing Huh-7 and Hep3B2.1-7 cells were successfully constructed (both P<0.01), and knockdown of KIF2C expression significantly inhibited the proliferative (all P<0.01), invasive and migratory (all P<0.01) capacities of Huh-7 and Hep3B2.1-7 cells, and the conditioned culture medium of HCC cells with knockdown of KIF2C expression could significantly inhibit the angiogenic capacity of HUVEC cells in vitro (P<0.05 or P<0.01). Conclusion: KIF2C promotes the ability of Huh-7 and Hep3B2.1-7 cells to proliferate, invade and migrate as well as HUVEC angiogenesis, suggesting that KIF2C may be a potential target for the treatment of HCC. [ABSTRACT FROM AUTHOR]

AIM: To investigate the effects of adipose-derived stem cells （ADSCs） with overexpression or silencing of long noncoding RNA（ lncRNA） SNHG8 on the viability, migration, angiogenesis, and the expression of vasoactive factors in human umbilical vein endothelial cells （HUVECs）. METHODS: Identification of ADSCs derived from morbidly obese patients （O-ADSCs） was conducted using flow cytometry and induction of lipogenesis and osteogenesis. The expression of lncRNA SNHG8 in healthy human ADSCs （H-ADSCs） and O-ADSCs was detected by RT-qPCR. Transwell method was used to establish the indirect co-culture system of ADSCs and HUVECs for 48 h, and the cells were divided into O-ADSCs+HUVECs group, H-ADSCs+HUVECs group, and HUVECs alone group. The mRNA and protein expression levels of angiotensin II（ Ang II）, endothelin-1（ ET-1） and endothelial nitric oxide synthase（ eNOS） in HUVECs were detected by RT-qPCR and Western blot. The lncRNA SNHG8 overexpression and silencing lentiviruses were con-structed and used to infect O-ADSCs. The indirect co-cultured ADSCs and HUVECs were divided into O-ADSCs-OE-SNHG8+ HUVECs group, O-ADSCs-OE-NC+HUVECs group, O-ADSCs-sh-SNHG8+HUVECs group, and O-ADSCs-sh-NC+HUVECs group. After co-culture for 48 h, the viability, migration and tubule formation of HUVECs were detected by CCK-8, scratch and angiogenesis assays, respectively. The mRNA and protein expression levels of Ang II, ET-1 and eNOS in HUVECs were detected by RT-qPCR and Western blot, respectively. The nitrate reductase method was used to detect the content of NO in HUVECs. RESULTS:（ 1） The cultured cells were identified as ADSCs.（ 2） Compared with H-ADSCs, lncRNA SNHG8 expression was significantly up-regulated in O-ADSCs（ P<0. 01）.（ 3） Compared with H-ADSCs+HUVECs group and HUVECs group, the mRNA and protein expression levels of Ang II and ET-1 in HUVECs in O-ADSCs+HUVECs group were up-regulated（ P<0. 01）.（ 4） Overexpression of lncRNA SNHG8 in O-ADSCs enhanced the viability, migration and tube formation ability of HUVECs, up-regulated the mRNA and protein expression levels of Ang II and ET-1, down-regulated the mRNA and protein expression levels of eNOS, and decreased the content of NO in HUVECs （P< 0. 05）. However, silencing of lncRNA SNHG8 in O-ADSCs exerted opposite results （P<0. 05）. CONCLUSION: （1） The O-ADSCs can promote endothelial cell viability, migration and tubule formation through paracrine effects.（ 2） The OADSCs with overexpression of lncRNA SNHG8 promote the imbalance of diastolic and contractile factors secreted by endothelial cells, and induce the dysfunction of vascular endothelial cells. [ABSTRACT FROM AUTHOR]

Aim To investigate the mechanism and signal pathways of xeroderma pigmentosum group D(XPD) gene on the proliferation of human umbilical vein smooth muscle cell (HUVSMC) induced by ox-LDL. Methods HUVSMCs were transfected with the plasmids of pEGFP-N2/XPD using Lipofectamine 2000, and subsequently silent mTOR gene. MTT and EdU assay was used to detect the cell proliferation. Flow cytometry was used to examine the cell apoptosis. The expression of XPD, lectin-like oxidized low-density lipoprotein receptor 1(LOX-1), mTOR, phosphomTOR, Bcl-2 and Bax was measured by Western blot. Results The expression of XPD and Bax protein was downregulated in ox-LDL group (P<0. 05), while the expression of LOX-1, mTOR, Bcl-2 protein and the ratio of Bcl-2/Bax was significantly up-regulated (P<0. 05), compared with control group. Cell proliferation of ox-LDL group increased obviously (P<0. 05). After transfected with the pEGFP-N2/XPD plasmid, the expression of Bax was significantly up-regulated, while the expression of LOX-1, mTOR, Bcl-2 and the ratio of Bcl-2/Bax were significantly down-regulated (P< 0. 05). Flow cytometry showed that overexpression of XPD increased the apoptosis rate of HUVSMC (P<0. 05). MTT and BdU showed that cell proliferation of pEGFP-N2/XPD group reduced compared with control group (P<0. 05). Compared with control group, the expression of LOX-1 was significantly down-regulated in siRNA mTOR group (P<0. 05). Conclusion XPD can inhibit HUVSMC proliferation and promote its apoptosis, and reduce the effect of ox-LDL promoting proliferation of HUVSMC via the mTOR/LOX-1 pathway. XPD may be the target of treatment of atherosclerosis. [ABSTRACT FROM AUTHOR]

Objective To evaluate the changes in vitamin D levels in patients with intrahepatic cholestasis of pregnancy (ICP) and to analyze the correlation between vitamin D and total bile acids (TBA) levels. Methods A total of 60 pregnant women were selected (30 in the normal group and 30 in the ICP group) . Demographic characteristics and perinatal data were recorded and collected. Serum TBA concentration, liver function, total cholesterol, triglyceride and serum 25 (OH) D levels were measured. Results No significant differences were observed in maternal age at pregnancy, body mass index (BMI）, ALT, AST, γ-glutamyltransferase levels between two groups (all P > 0.05) . The Apgar scores at 5 minutes of all newborn infants were 10. In the ICP group, the gestational age of pregnant women was younger and the birth weight of newborn infants was lower compared with those in normal group (both P < 0.05) . Serum 25 (OH) D level was (24.84±1.88）μg/L in the ICP group, lower than (31.72±2.39）μg/L in the normal group (P < 0.05) . In the ICP group, 25 (OH) D level in the umbilical vein blood was (13.61±1.24）μg/L, lower compared with (21.96±2.69）μg/L in the normal group (P < 0.01) . The 25 (OH) D level in the umbilical vein blood was positively correlated with serum 25 (OH) D level in pregnant women in both groups (normal group： r=0.763, P < 0.001； ICP group：r=0.726, P < 0.001）. In the ICP group, serum 25 (OH) D level was negatively correlated with TBA level in the ICP group (r=-0.692, P < 0.001）. There was no correlation between serum 25 (OH) D and TBA levels in normal pregnant women (P > 0.05) . There was no significant differences in serum total cholesterol and triglyceride levels between two groups (both P > 0.05) . Conclusions The vitamin D levels in serum and umbilical vein blood of pregnant women in the ICP group are lower than those of normal pregnant women, which may be related to high TBA level in ICP patients. For ICP pregnant women, supplemental dose of vitamin D may be appropriately increased to promote intrauterine development. [ABSTRACT FROM AUTHOR]

BACKGROUND: MiR-126-3p from adipose-derived mesenchymal stem cells released exosomes (AMSC-Exos) has been used as a potential biomarker of diabetes, but few studies of glucolipotoxicity and mechanism of miR-126-3p on human umbilical vein endothelial cells are found. OBJECTIVE: To explore the effect and mechanism of miR-126-3p from AMSC-Exos on glucolipotoxicity of human umbilical vein endothelial cells. METHODS: (1) Glucolipotoxicity model of human umbilical vein endothelial cells was induced by 30 mmol/L glucose and 100 μmol/L palmitic acid in vitro. (2) The supernatant of passage 4 AMSC-Exos was collected. The morphology of AMSC-Exos was observed by transmission electron microscope. The size distribution of AMSC-Exos was determined by nanoparticle tracking analysis. (3) Human umbilical vein endothelial cells with glucolipotoxicity were treated with AMSC-Exos. The content of reactive oxygen species and apoptosis rate were detected by flow cytometry. ELISA was implemented to detect the expression of inflammatory factors. (4) RT-qPCR was used to detect the expression levels of miR-126-3p mRNA in AMSC-Exos and normal human umbilical vein endothelial cells co-cultured with AMSC. (5) miR-126-3p overexpression was transfected into human umbilical vein endothelial cells. Cell proliferation was detected by CCK- 8 assay. Western blot assay was used to detect the expression levels of apoptotic proteins. (6) The target genes of miR-126-3p were predicted and verified by bioinformatics software. Dual luciferase reporter gene assay was applied to verify and predict signaling pathway. (7) CRK overexpression was transfected into human umbilical vein endothelial cells with glucolipotoxicity. The expression levels of apoptotic protein and p-AKT were detected by western blot assay. (8) Human umbilical vein endothelial cell glucolipotoxicity model was co-treated with AKT pathway inhibitor RG7440 and miR-126-3p overexpression/AMSC-Exos. Apoptotic protein expression was detected by western blot assay and apoptosis rate was detected by flow cytometry. RESULTS AND CONCLUSION: (1) AMSC-Exos were round or oval membranous vesicles, and the particle size ranged from 30 to 200 nm. (2) Compared with the model group, AMSC-Exos could remarkably reduce the expression levels of interleukin-1β, interleukin-6 and interleukin-8 (P < 0.05, P < 0.001), and obviously reduced the reactive oxygen species and cell apoptosis rate (P < 0.05). (3) Compared with adipose-derived mesenchymal stem cells, mRNA expression level of miR-126- 3p from AMSC-Exos was significantly increased (P < 0.001). Compared with human umbilical vein endothelial cells, co-culture with adipose-derived mesenchymal stem cells could significantly increase the expression level of miR-126-3p of human umbilical vein endothelial cells (P < 0.001). (4) miR-126-3p overexpression could significantly promote cell proliferation, reduce cell apoptotic rate and expression levels of cleaved caspase 3, 9 (P < 0.01, P < 0.001). (5) Bioinformatics analysis and dual luciferase reporter gene assay proved that CRK was the target gene of miR-126-3p. The AKT pathway was as the object of next experimental research. (6) CRK overexpression could activate AKT pathway and up-regulate expression level of cleaved caspase 3, 9. Compared with the Exos group, the cell apoptosis rate was significantly higher in the Exos + AKT inhibitor group (P < 0.001). (7) The results showed that miR-126-3p from AMSC-Exos could improve the glucolipotoxicity of human umbilical vein endothelial cells. It is supposed that the mechanism maybe work by miR-126-3p regulating the AKT pathway via targeting CRK gene. [ABSTRACT FROM AUTHOR]

Copyright of Food Research & Development is the property of Food Research & Development Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Vascular endothelial cells are the main target of arsenic toxicity and the molecular mechanism of arsenic-induced endothelial cell injury needsto be further studied. OBJECTIVE: To study the effects of sodium arsenite on human umbilical vein endothelial cell injury and sphingosine kinase 1/sphingosine 1-phosphate signaling axis of human umbilical vein endothelial cells. METHODS: Human umbilical vein endothelial cells were isolated, cultured, and identified. The cells were treated with 0, 5, 10, 15, 20, 25 µmol/L sodium arsenite for 24 hours. Cell viability was detected by cell counting kit-8. Cell morphology was observed by inverted phase contrast microscope. The content of intracellular reactive oxygen species was detected by fluorescent probe DCFH-DA. Annexin V-FITC/PI double labeling combined with flow cytometry and TUNEL were used to detect apoptosis. The content of sphingosine 1-phosphate in cells was detected by ELISA. The mRNA and protein expressions of vascular cell adhesion molecule-1, sphingosine kinase 1, and sphingosine 1-phosphate were detected by real-time fluorescence quantitative PCR and western blot respectively. RESULTS AND CONCLUSION: Compared with the control group (0 µmol/L sodium arsenite), the cell viability decreased gradually along with the increased concentration of sodium arsenite in a dose-dependent manner; the cell fusion rate decreased gradually, the cell gap widened gradually, and the number of exfoliated and floating cells increased gradually; the reactive oxygen species content and apoptosis rate increased gradually; the sphingosine 1-phosphate content in cells increased gradually; the relative mRNA and protein expressions of vascular cell adhesion molecule-1 and sphingosine kinase 1 increased gradually, but the relative mRNA and protein expression of sphingosine kinase 1 decreased gradually. To conclude, sodium arsenite-injured human umbilical vein endothelial cell injury may be related to the activation of sphingosine kinase 1/sphingosine 1-phosphate signaling axis and the downregulation of sphingosine 1-phosphate receptor 1. Sphingosine kinase 1/sphingosine 1-phosphate signaling axis may become a new target of arsenic-induced cardiovascular injury. [ABSTRACT FROM AUTHOR]

AIM: To investigate the mechanism and the protective effect of matrine against hydrogen peroxide (H2O2) -induced oxidative injury in human umbilical vein endothelial cells (HUVECs) based on the KLF4/Nrf2 pathway. METHODS: The HUVECs were cultured and screened to determine the experimental concentration of matrine using CCK-8 method. The HUVECs were divided into control group, model group, and low-, medium- and high-concentration (0.5, 1 and 2 mmol/L) matrine groups. An oxidative injury model of HUVECs was induced by H2O2 (0.5 mmol/L), and cell viabilty and intracellular reactive oxygen species (ROS), malondialdehyde(MDA), superoxide dismutase (SOD) and glutathione peroxidase(GPX)levels were detected. The mRNA and protein levels of Kriippel-like factor 4(KLF4), nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), quinone oxidoreductase 1(NQO1) and y-glutamyl cysteine synthetase (y-GCS) were detected using RT-qPCR and Western blot. Changes in these indicators were observed after siRNA-mediated knockdown of KLF4 gene expression and cotreatment with matrine. RESULTS: Compared with model group, the cell viability was increased (P<0. 05), ROS and MDA levels were decreased (PVO. 05), SOD and GPX activity was increased (PVO. 05), and the expression levels of KLF4, NRF2, HO-1, NOQI and y-GCS were increased in matrine groups（PV0. 05）. Inhibiting KLF4 expression significantly weakened the protective effect of matrine against H2O2- induced decrease in cell viability, increase in ROS, and expression of oxidative stress-related molecules（PV0. 05）. CONCLUSION: Matrine can alleviate H2O2-induced oxidative injury in HUVECs by activating KLF4/Nrf2 pathway and inhibiting oxidative stress. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

OBJECTIVE: To investigate whether sweroside regulates hypertension-induced vascular endothelial dysfunction by regulating Forkhead box O1 (FOXO1) expression. METHODS: (1) In vivo: The renal aorta constriction method was used to establish a hypertensive rat model. Forty male Sprague-Dawley rats were randomly divided into four groups: sham group, hypertension group, hypertension+25 mg/kg sweroside group, and hypertension+50 mg/kg sweroside group. TUNEL staining was used to detect the apoptosis of rat thoracic aorta endothelial cells. (2) In vitro: 50 μmol/L H2O2 was used to stimulate human umbilical vein endothelial cells to establish a cell oxidative damage model. Damaged cells were divided into control group, H2O2 group, H2O2+10, 20, or 40 μmol/L sweroside groups, H2O2+Vector group (negative control), H2O2+pcDNA-FOXO1 group, H2O2+40 μmol/L sweroside+Scramble group (negative control), and H2O2+40 μmol/L sweroside+si-FOXO1 group. MTT and flow cytometry were used to detect cell proliferation and apoptosis, respectively. ELISA was used to detect the levels of angiotensin II, malondialdehyde, and nitric oxide levels in rat serum and human umbilical vein endothelial cells, as well as vascular cell adhesion molecule 1, intercellular adhesion molecule 1, and E-selection levels in rat thoracic aorta tissues and human umbilical vein endothelial cells. RT-qPCR and western blot were used to detect the mRNA and protein expression of FOXO1 in rat thoracic aorta tissues and human umbilical vein endothelial cells. RESULTS AND CONCLUSION: (1) In vivo: compared with the sham group, blood pressure and apoptosis were significantly increased (P < 0.05), the expression levels of FOXO1 mRNA and protein were significantly reduced (P < 0.05), the contents of angiotensin II, malondialdehyde, vascular cell adhesion molecule 1, intercellular adhesion molecule 1, and E-selectin were significantly increased (P < 0.05), and the content of nitric oxide was significantly reduced (P < 0.05) in hypertensive rats. Sweroside could improve vascular dysfunction in hypertensive rats in a dose-dependent manner. (2) In vitro: compared with the control group, cell proliferation, FOXO1 expression and nitric oxide content were significantly reduced (P < 0.05), and cell apoptosis and malondialdehyde, vascular cell adhesion molecule 1, intercellular adhesion molecule 1, and E-selection contents were significantly increased (P < 0.05) in the H2O2 group. Sweroside treatment or FOXO1 overexpression could improve the dysfunction of human umbilical vein endothelial cells induced by H2O2, and the interference of FOXO1 could reverse the effect of sweroside. To conclude, sweroside can improve vascular endothelial dysfunction in hypertensive rats by promoting FOXO1 expression. [ABSTRACT FROM AUTHOR]

Objective We aimed to explore the protective effect of Qingre Zhixue Formula and tripterygium wilfordii multiglucoside on the endothelial damage induced by serum-derived poly IgA in patients with Henoch-Schönlein purpura nephritis and its effect on the expression of key proteins of the NF-κB signaling pathway. Methods A total of 80 patients with Henoch-Schönlein purpura nephritis from The First Affliated Hospital of Henan University of Chinese Medicine and 38 healthy controls were enrolled in this study. Serum IgA was purified from all participants in order to prepare serum-derived poly IgA. Moreover, 60 Sprague-Dawley rats were divided into the following five groups (n = 12 rats per group): the Qingre Zhixue Formula group (31. 25 mg/ kg), the tripterygium wilfordii multiglucoside group (46. 88 mg/ kg), the combined group (31. 25 mg/ kg + 46. 88 mg/ kg), the prednisone acetate group (23. 44 mg/ kg) and the saline group. Rats in each group were gavaged twice a day for 7 days. Additionally, human umbilical vein endothelial cells (HUVECs) were stimulated with serum-derived poly IgA (200 µg/ mL) derived from patients with Henoch-Schönlein purpura nephritis for 24 h to construct HUVECs injury model. The cells were divided into the following seven groups: the blank group, the healthy group, the model group, the Qingre Zhixue Formula group, the tripterygium wilfordii multiglucoside group, the combined group and the prednisone acetate group, and provide corresponding intervention. siRNA transfection was used to inhibit the NF-κB signaling pathway, and divide the transfected cells into the blank group, the model group, the model+normal control group, the model+ transfection group, the Qingre Zhixue Formula group, the tripterygium wilfordii multiglucoside group, the combined group and the prednisone acetate group. Cell viability was detected by the MTT assay, the apoptosis rate was detected by flow cytometry, and the protein expression levels of p-P65, p-P50, IKKβ, and IκBα were detected by Western blotting before and after transfection. Results Compared with the blank group, the cell viability of the model group was decreased (P<0. 05). Compared with the model group, the cell viability of each treatment group was increased (P<0. 05). Compared with the combined group, the cell viability of the Qingre Zhixue Formula group, the tripterygium wilfordii multiglucoside group, and the prednisone acetate group was decreased (P<0. 05). Compared with the blank group, the protein expression levels of p-P65, p-P50 and IKKβ in the model group were increased (P<0. 05), and the protein expression level of IκBα was decreased (P <0. 05). Compared with the model group, the protein expression levels of p-P65, p-P50 and IKKβ were decreased in each group (P<0. 05), and the protein expression level of IκBα was increased (P <0. 05). Compared with the combined group, the protein expression levels of p-P65, p-P50, and IKKβ in the Qingre Zhixue Formula group, the tripterygium wilfordii multiglucoside group and the prednisone acetate group were increased (P<0. 05), while the protein expression level of IκBα was decreased ( P < 0. 05). After siRNA transfection, compared with the blank group, the protein expression levels of p-P65, p-P50 and IKKβ in the model group and the model+normal control group were increased (P<0. 05), and the protein expression level of IκBα was decreased (P<0. 05). Compared with the model group, the protein expression levels of p-P65, p-P50 and IKKβ were decreased (P<0. 05), and the protein expression level of IκBα was increased (P< 0. 05) in the cells of the model+transfection group, the Qingre Zhixue Formula group, the tripterygium wilfordii multiglucoside group, the combined group and the prednisone acetate group. Conclusion Qingre Zhixue Formula combined with tripterygium wilfordii multiglucoside may inhibit the activation of the NF-κB pathway to improve the cell viability of HUVECs induced by serum-derived poly IgA in children with Henoch-Schönlein purpura nephritis, so it plays a role in protecting endothelial cells. [ABSTRACT FROM AUTHOR]

BACKGROUND: High density polyethylene has been widely used as a repair material for cranial and maxillofacial bone defects, but its preparation method and surface activity still need further improvement. OBJECTIVE: To optimize the preparation method of high density polyethylene and improve the surface activity of high density polyethylene. METHODS: The high density polyethylene scaffolds were prepared by extrusion 3D printing technology, and the scaffolds were immersed in dopamine solution and simulated body fluid successively to be coated with polydopamine and hydroxyapatite. The microstructure, hydrophilicity and compression modulus of the scaffolds before and after coating were characterized. Mouse embryonic osteogenic precursor cells (MC3T3-E1) and human umbilical vein endothelial cells were inoculated on the surface of the scaffold to evaluate the cytocompatibility and early osteogenic and angiogenic differentiation of the scaffold before and after coating. RESULTS AND CONCLUSION: (1) The 3D printed high density polyethylene scaffold’s fibers were arranged regularly and pores were uniform. Characterization results showed that polydopamine and hydroxyapatite coatings were successful on the surface of the scaffolds. Compared with the unmodified scaffold, the surface water contact angle of the scaffold modified with polydopamine coating and polydopamine + hydroxyapatite coating decreased significantly (P < 0.05), and the compressive modulus did not change significantly. (2) Compared with the unmodified scaffold, the modified scaffold with polydopamine coating and polydopamine + hydroxyapatite coating could promote the adhesion of MC3T3-E1 cells and human umbilical vein endothelial cells (P < 0.05). The cell adhesion promoting effect of double coating modified group was better than that of single coating modified group (P < 0.05). Compared with the unmodified scaffold, the modified scaffold with polydopamine coating and polydopamine + hydroxyapatite coating could promote the proliferation of MC3T3-E1 cells and human umbilical vein endothelial cells (P < 0.05). The proliferation promoting effect of double coating modified group was better than that of single coating modified group (P < 0.05). Compared with unmodified scaffolds, the scaffolds modified with polydopamine coating and polydopamine + hydroxyapatite coating could promote the osteogenic differentiation of MC3T3-E1 cells (P < 0.05), and increase the expression of angiogenic factor CD31 in human umbilical vein endothelial cells. The double-coating modified group was more obvious. (3) The results showed that the high density polyethylene scaffolds coated with polydopamine and hydroxyapatite based on 3D printing technology have good cytocompatibility and early osteogenic and angiogenic differentiation ability. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Contemporary Pediatrics is the property of Xiangya Medical Periodical Press and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Aim To investigate the relationship between apolipoprotein E (ApoE) receptor 2 (ApoER2) degradation by proprotein convertase subtilisin kexin 9 (PCSK9) and the anti-inflammatory effect of ApoE/ApoER2. Methods Human umbilical vein endothelial cells (HUVEC) and HepG2 cells were cultured in vitro, Western blot and ELISA were used to detect the effects of lipopolysaccharide (LPS) on the expression and secretion of Toll-like receptor (TLR4), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and PCSK9 in HUVEC; the effects of ApoE3 on the expression and secretion of TNF-α, IL-6, PCSK9 and ApoER2 in HUVEC induced by LPS; the effects of three isoforms of ApoE (ApoE2, ApoE3 and ApoE4) on the expression of PCSK9 and ApoER2 in HUVEC and HepG2 cells under non-inflammatory conditions; and the effects of PCSK9 on the expression and secretion of ApoER2, TNF-α and IL-6 in HUVEC. Results Western blot and ELISA showed that LPS up-regulated the expression and secretion of TLR4, TNF-α, IL-6 and PCSK9 in HUVEC; ApoE3 inhibited LPS-induced inflammatory responses, and up-regulated ApoER2 expression and secretion; the three isoforms of ApoE (ApoE2, ApoE3 and ApoE4) had no effect on the expression of PCSK9 and ApoER2 in HUVEC and HepG2 cells under non-inflammatory conditions. Different doses (0, 0. 5, 1. 0 and 2. 5 mg/L) of recombinant human PCSK9 were used to treat HUVEC for 24 h, Western blot and ELISA showed that PCSK9 up-regulated the ex-pression and secretion of TNF-α and IL-6, and down-regulated the expression of ApoER2. Conclusion PCSK9 antagonizes the anti-inflammatory effects of ApoE/ApoER2 by degrading ApoER2. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of omega-3 fatty acids on the invasion and angiogenesis of human trophoblast cells (HTR-8/SVneo). Methods: Different concentrations of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) groups were set up: 0 μmol/L EPA group, 1 μmol/L EPA group, 50 μmol/L EPA group and 100 μmol/L EPA group; 0 μmol/L DHA group, 1 μmol/L DHA group, 50 μmol/L DHA group and 100 μmol/L DHA group. The HTR-8/SVneo cells in each group were cultured with corresponding concentrations of EPA and DHA for 48 h. Then the cell proliferation was detected by the CCK-8 method, and the cell invasion was detected by the Matrigel Transwell test. Human umbilical vein endothelial cells (HUVEC) were cultured for 6 h with the supernatant of HTR-8/SVneo cells treated with EPA and DHA, and then the tubule forming ability of HUVEC was detected. The expression level of tripartite motif-containing 22 (TRIM22), signal transducer and activator of transcription 1 (STAT1), p-STAT1 (Tyr701), matrix metalloproteinase 2 (MMP2), MMP9, MMP9 and VEGF in HTR-8/SVneo cells were detected by qRT-PCR and Western blot. Results: Compared with the 0 μmol/L EPA group or 0 μmol/L DHA group, OD450 nm, number of invaded cells, and relative protein expression level of MMP2 and MMP9 in the 50 μmol/L EPA group, 100 μmol/L EPA group, 50 μmol/L DHA group and100 μmol/L DHA group were increased (P＜0.05). Compared with the 0 μmol/L EPA group or 0 μmol/L DHA group, the relative tubule length and the relative expression of VEGF protein in the 50 μmol/L EPA group, 100 μmol/L EPA group, 50 μmol/L DHA group and100 μmol/L DHA group were increased (P＜0.05). Compared with the 0 μmol/L EPA group or 0 μmol/L DHA group, the relative expression levels of TRIM22 m RNA and protein in the 50 μmol/L EPA group, 100 μmol/L EPA group, 50 μmol/L DHA group and 100μmol/L DHA group were increased, while the relative expression of STAT1 m RNA and p-STAT1 (Tyr701) protein were decreased (P＜0.05). Conclusion: Omega-3 fatty acid treatment can promote the invasiveness and angiogenesis of trophoblast cells. The mechanism may be related to the up-regulation of TRIM22 and the inhibition of STAT1 activity. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: With the continuous development of three-dimensional (3D) printing technology and bone tissue engineering, more and more 3D printed scaffolds have applied in study of bone tissue engineering. The 3D printed scaffold with hollow pipe structure has the advantages of vascular growth and nutrient delivery, which is worthy of further study. OBJECTIVE: To investigate the effect of ionic components released by akermanite on osteogenic differentiation of rat bone marrow mesenchymal stem cells and migration of human umbilical vein endothelial cells and fabricate the 3D-printed akermanite scaffold with hollow-pipe structure with coaxial 3D printing technology. METHODS: The rat bone marrow mesenchymal stem cells and human umbilical vein endothelial cells were cultured with different concentrations of akermanite extracts (1/4, 1/8 and 1/16). The proliferation of rat bone marrow mesenchymal stem cells was detected by CCK-8 assay. Osteogenic differentiation of human umbilical vein endothelial cells was investigated by alkaline phosphatase staining and RT-qPCR. Transwell assay was used to observe the migration of human umbilical vein endothelial cells in response to different concentrations of akermanite extracts. The akermanite scaffold with hollow-pipe structure was prepared using a modified printer nozzle with a core/shell structure with the printing system. The scaffolds were immersed into deionized water and the extracts were collected at set time points. The concentration of ionic products was detected with inductively coupled plasma atomic emission spectrometry. RESULTS AND CONCLUSIOIN: (1) CCK-8 assay indicated that the akermanite extracts had a concentration and time-related effect on promoting the proliferation of bone marrow mesenchymal stem cells. (2) Alkaline phosphatase staining showed that the akermanite extracts had a concentration-related effect on the alkaline phosphatase activity of rat bone marrow mesenchymal stem cells. RT-qPCR indicated that the extracts had a concentration-related effect on the mRNA expression of alkaline phosphatase, collagen-1 and Runx2 of bone marrow mesenchymal stem cells. (3) The akermanite extracts had a concentration-related effect on the migration of human umbilical vein endothelial cells. (4) The scaffolds would continuously release the Ca, Mg and Si ions during immersion into deionized water for 30 days. The akermanite scaffold with hollow pipes was conducive to the release of biologically active ions and had high concentration. (5) The result showed that the akermanite scaffolds with hollow pipes were successfully prepared with the modified 3D printer. The ionic products released by scaffolds had an obvious effect on osteogenesis of rat bone marrow mesenchymal stem cells and promoted migration of human umbilical vein endothelial cells, thereby accelerating vascular regeneration. [ABSTRACT FROM AUTHOR]

BACKGROUND: Preliminary work has found that homocysteine accelerates the aging of umbilical vein endothelial cells through reactive oxygen species. This experiment preliminarily studies the relevant mechanisms affecting endothelial cell aging. OBJECTIVE: To investigate the effects of echinacoside on the expression of cytoplasmic polyadenylate binding protein 1 (CPEB1), sirtuin1 (SIRT1), P53 and P21 genes in human umbilical vein endothelial cells. METHODS: Human umbilical vein endothelial cells were cultured in vitro. D-galactose 10 g/L was used to construct cell aging model. The proliferation viability of cells treated with echinacoside (0, 10, 20, 50, 100, 200, 300, 400, 500 mg/L) for 12 and 24 hours was analyzed by CCK-8 assay, and the optimal mass concentration and intervention time of echinacoside were screened. Human umbilical vein endothelial cells were divided into normal control group, D-galactose group and echinacoside groups (100, 200, and 300 mg/L). β-Galactosidase staining was used to detect the positive staining rate of cells after echinacoside pre-intervention for 12 hours. Real time RT-PCR and western-blot assay were used to detect the mRNA expression levels of CPEB1, Sirt1, P53 and P21 and the protein expression levels of CPEB1, Sirt1 and P21 in human umbilical vein endothelial cells after echinacoside pretreatment for 12 hours. RESULTS AND CONCLUSION: (1) The results of CCK-8 assay showed that the survival rate of echinacoside group at 12 hours was significantly higher than that at 24 hours. Compared with the D-galactose group, cell viability increased in the echinacoside 100, 200, and 300 mg/L groups to varying degrees (P < 0.000 1), and there was a significant difference among the three groups (P < 0.01). (2) Compared with the normal control group, the D-galactose group had the highest positive rate of β-galactosidase staining (P < 0.0001). 100, 200, and 300 mg/L echinacoside pretreatment for 12 hours could reduce the positive rate of β-galactosidase staining to a certain extent (P < 0.000 1). (3) Compared with the normal control group, the mRNA expression levels of CPEB1, P53 and P21 were increased (P < 0.000 1), and the expression level of SIRT1 mRNA was decreased (P < 0.000 1) in the D-galactose group. Compared with the D-galactose group, 100, 200, and 300 mg/L echinacoside pretreatment for 12 hours decreased the mRNA expression levels of CPEB1, P53, and P21 (P < 0.000 1), but increased Sirt1 mRNA expression (P < 0.000 1). Western blot assay results were consistent with real-time fluorescence quantitative polymerase chain reaction results. (4) These findings indicate that echinacoside may delay D-galactose-induced human umbilical vein endothelial cell senescence by down-regulating CPEB1 and P53/ P21 expression levels and up-regulating Sirt1 expression levels. [ABSTRACT FROM AUTHOR]

BACKGROUND: MiR-126-3p from adipose-derived mesenchymal stem cells released exosomes (AMSC-Exos) has been used as a potential biomarker of diabetes, but few studies of glucolipotoxicity and mechanism of miR-126-3p on human umbilical vein endothelial cells are found. OBJECTIVE: To explore the effect and mechanism of miR-126-3p from AMSC-Exos on glucolipotoxicity of human umbilical vein endothelial cells. METHODS: (1) Glucolipotoxicity model of human umbilical vein endothelial cells was induced by 30 mmol/L glucose and 100 μmol/L palmitic acid in vitro. (2) The supernatant of passage 4 AMSC-Exos was collected. The morphology of AMSC-Exos was observed by transmission electron microscope. The size distribution of AMSC-Exos was determined by nanoparticle tracking analysis. (3) Human umbilical vein endothelial cells with glucolipotoxicity were treated with AMSC-Exos. The content of reactive oxygen species and apoptosis rate were detected by flow cytometry. ELISA was implemented to detect the expression of inflammatory factors. (4) RT-qPCR was used to detect the expression levels of miR-126-3p mRNA in AMSC-Exos and normal human umbilical vein endothelial cells co-cultured with AMSC. (5) miR-126-3p overexpression was transfected into human umbilical vein endothelial cells. Cell proliferation was detected by CCK- 8 assay. Western blot assay was used to detect the expression levels of apoptotic proteins. (6) The target genes of miR-126-3p were predicted and verified by bioinformatics software. Dual luciferase reporter gene assay was applied to verify and predict signaling pathway. (7) CRK overexpression was transfected into human umbilical vein endothelial cells with glucolipotoxicity. The expression levels of apoptotic protein and p-AKT were detected by western blot assay. (8) Human umbilical vein endothelial cell glucolipotoxicity model was co-treated with AKT pathway inhibitor RG7440 and miR-126-3p overexpression/AMSC-Exos. Apoptotic protein expression was detected by western blot assay and apoptosis rate was detected by flow cytometry. RESULTS AND CONCLUSION: (1) AMSC-Exos were round or oval membranous vesicles, and the particle size ranged from 30 to 200 nm. (2) Compared with the model group, AMSC-Exos could remarkably reduce the expression levels of interleukin-1β, interleukin-6 and interleukin-8 (P < 0.05, P < 0.001), and obviously reduced the reactive oxygen species and cell apoptosis rate (P < 0.05). (3) Compared with adipose-derived mesenchymal stem cells, mRNA expression level of miR-126- 3p from AMSC-Exos was significantly increased (P < 0.001). Compared with human umbilical vein endothelial cells, co-culture with adipose-derived mesenchymal stem cells could significantly increase the expression level of miR-126-3p of human umbilical vein endothelial cells (P < 0.001). (4) miR-126-3p overexpression could significantly promote cell proliferation, reduce cell apoptotic rate and expression levels of cleaved caspase 3, 9 (P < 0.01, P < 0.001). (5) Bioinformatics analysis and dual luciferase reporter gene assay proved that CRK was the target gene of miR-126-3p. The AKT pathway was as the object of next experimental research. (6) CRK overexpression could activate AKT pathway and up-regulate expression level of cleaved caspase 3, 9. Compared with the Exos group, the cell apoptosis rate was significantly higher in the Exos + AKT inhibitor group (P < 0.001). (7) The results showed that miR-126-3p from AMSC-Exos could improve the glucolipotoxicity of human umbilical vein endothelial cells. It is supposed that the mechanism maybe work by miR-126-3p regulating the AKT pathway via targeting CRK gene. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Preventive Veterinary Medicine / Zhongguo Yufang Shouyi Xuebao is the property of Chinese Journal of Preventive Veterinary Medicine Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Modern Food Science & Technology is the property of Editorial Office of Modern Food Science & Technology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objectives: To investigate the rate and risk factors of tip displacement of umbilical venous catheterization (UVC) in preterm infants. Methods: This was a multicenter cohort study. Study population were preterm infants admitted to 44 tertiary hospitals in China between October 2019 and August 2021. Demographic information, general clinical data, UVC indwelling conditions and related complications were collected. The primary outcome was the rate of UVC tip displacement. The observation time points were 2 d and 7 d after UVC. They were grouped according to UVC displacement, gestational age, and birth weight. Binary Logistic regression was used to analyze the risk factors of UVC tip displacement. Results: The 2 086 preterm infants had a gestational age of (29.9±2.3) weeks and a birth weight of (1 248±298) g. There were 1 106 male preterm infants (53.0%). The rate of UVC displacement at 2 d and 7 d were 34.6% (721/2 086) and 33.6% (494/1 470), respectively, with no statistically significant difference ( χ 2 =0.35, P =0.533). Univariate analysis indicated that male infants, small gestational age, low birth weight and small catheter diameter were all risk factors for UVC tip displacement at the 2 d time point (all P <0.05). Multivariate analysis showed that small catheter diameter was an independent risk factor for tip displacement at both 2 d ( OR= 0.47, 95% CI 0.34-0.66) and 7 d ( OR= 0.39, 95% CI 0.25-0.59) time points (both P <0.001). Conclusions: The rate of UVC tip displacement is high in preterm infants. It should be avoided to deliberately select a small diameter catheter for UVC, and pay attention to the imaging monitoring of the tip position after UVC.

BACKGROUND: Porphyromonas gingivalis infection is a risk factor that has been found to be related to atherosclerosis and other diseases in recent years. However, different fimA genotypes of Porphyromonas gingivalis have different pathogenic abilities. Actively explore Porphyromonas gingivalis high-risk bacterial strains play an important role in improving the diagnosis and treatment mechanism of atherosclerosis. OBJECTIVE: To investigate the effects of different fimA genotypes of Porphyromonas gingivalis on the secretion of monocyte chemoattractant protein-1, interleukin-6, and endothelin-1/nitric oxide in human umbilical vein endothelial cells. METHODS: Porphyromonas gingivalis genotypes IV, II, and I fimA were cultured under anaerobic conditions, and the multiplicity of infection was 100 to infect human umbilical vein endothelial cells. In the positive control group, Porphyromonas gingivalis lipopolysaccharide was used to stimulate human umbilical vein endothelial cells, and in the negative control group, human umbilical vein endothelial cells were cultured with cell culture medium only. Enzyme-linked immunosorbent assay was used to detect the levels of monocyte chemoattractant protein 1, interleukin 6, endothelin 1/nitric oxide in the culture supernatant of human umbilical vein endothelial cells after 2, 6, and 24 hours in each group. RESULTS AND CONCLUSION: Except for the negative control group, the levels of interleukin 6, endothelin 1/nitric oxide, and monocyte chemoattractant protein 1 in the culture supernatant of human umbilical vein endothelial cells in the other four groups gradually increased. The levels of interleukin 6, endothelin 1/ nitric oxide in the IV fimA genotype stimulation group were higher than those in the II and I fimA genotype stimulation groups and the positive control group and the negative control group (P < 0.05). The level of monocyte chemoattractant protein 1 in the II fimA genotype stimulation group was higher than that in the IV, I fimA genotype stimulation group and the negative control group (P < 0.05). The results indicate that there are certain differences in the dysfunction mechanisms of Porphyromonas gingivalis with different fimA genotypes in stimulating human umbilical vein endothelial cells. The II fimA genotype and IV fimA gene have a strong ability to up-regulate the secretion of monocyte chemoattractant protein 1, interleukin 6, and endothelin 1/nitric oxide, and may play a dominant role in causing vascular vein endothelial cell dysfunction. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Chinese Institute of Food Science & Technology / Zhongguo Shipin Xuebao is the property of Journal of Chinese Institute of Food Science & Technology Periodical Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: There is a lack of perfect vascular system in tissue-engineered bone, among which vascularization is the key to limit its wide application. Appropriate matrix chemistry and fluid shear stress stimulation can promote the proliferation, differentiation and function of vascular endothelial cells, and guide the design and fabrication of scaffold materials. OBJECTIVE: To explore the effects of different chemical functional groups and fluid shear stress （FSS） on human umbilical vein endothelial cells, in order to find an efficient combination of material chemistry and fluid shear stress on human umbilical vein endothelial cells. METHODS: Self assembled monolayers with OH,CH3 and NH2 as end functional groups were prepared as matrix materials and blank glass as control.Human umbilical vein endothelial cells were seeded on the surface of four groups of glasses.The release of ATP within 15 minutes after culture and NO within 1 hour after culture was detected.The expression of endothelial nitric oxide synthase protein was detected by western blotting. The formation of focal adhesion and F-actin was observed by laser confocalicro scopy. Human umbilical vein endothelial cells were seeded on the surface of four groups of glasses. When the cells fused to 80%,they were loaded with 1.5 N/m² FSS for 1 hour. ATP release was detected within 15 minutes after loading, and NO release was detected within 1hour after loading. The expression of endothelial nitric oxide synthase was detected by western blotting after loading for 1 hour. RESULTS AND CONCLUSION:（1） Chemical stimulation had no effect on the release of ATP or NO, but FSS could increase the release of ATP and NO, and the expression of endothelial nitric oxide synthase. When FSS and material chemistry acted simultaneously, the expression of ATP and NO was closely related to material chemistry. The release of ATP and NO and the expression of endothelial nitric oxide synthase were highest in NH2-FSS group, followed by FSS group, and those in the CH3-FSS and OH-FSS groups were lowest.（2） Laser confocal microscope showed that a large number of focal adhesions and cytoskeleton protein F-actin could be detected in the NH2 group, followed by control group; those were least in the CH3 and OH groups.（3） The results showed that the combination of NH2 functional group and FSS produced high-efficiency response to shear stress, and the mechanism may be the formation of optimal focal adhesion and F-actin on NH2 surface [ABSTRACT FROM AUTHOR]

Previous studies believe that patent paraumbilical vein in cirrhotic portal hypertension can reduce portal venous flow, portal venous pressure, and the development of esophageal varices and esophageal variceal bleeding, but there are still controversies over this issue in clinical practice. This article reviews the formation of portal systemic collateral circulation, the characteristics of the paraumbilical vein, the definition and diagnosis of patent paraumbilical vein, and the influence of patent paraumbilical vein on the development of esophageal varices and esophageal variceal bleeding, and it is believed that patent paraumbilical vein may not reduce the development of esophageal varices and esophageal variceal bleeding. Contrary to the previous points of view, patent paraumbilical vein should be regarded as a manifestation of the progression of cirrhotic portal hypertension, which can lead to the complications such as hepatic encephalopathy, and therefore, targeted prevention measures should be adopted in clinical practice. [ABSTRACT FROM AUTHOR]

BACKGROUND: Endothelial dysfunction is an early predictor of atherosclerosis and cardiovascular disease. Umbilical cord mesenchymal stem cell transplantation provides the possibility for the treatment of vascular injury. OBJECTIVE: To explore the effect of overexpression of interleukin-8 receptor A/B on migration of human umbilical cord mesenchymal stem cells. METHODS: Primary cultured human umbilical cord mesenchymal stem cells and human umbilical vein endothelial cells were transfected with adenovirus vector containing interleukin-8 receptor A/B. Confocal immunofluorescence microscopy and western blot assay were used to observe the expression of interleukin-8 receptor A/B in cells. CCK-8 assay, competition test and adhesion test were used to detect the effects of interleukin-8 receptor A/B overexpression on cell proliferation, competitiveness and migration. RESULTS AND CONCLUSION: The fluorescent adenovirus vector overexpressing interleukin-8 receptor A/B has no significant effect on cell proliferation. However, the competition and migration abilities of human umbilical cord mesenchymal stem cells overexpressing interleukin-8 receptor A/B were significantly higher than those of human umbilical vein endothelial cells overexpressing interleukin-8 receptor A/B (P < 0.05). It is concluded that interleukin-8 receptor enhances the migration ability of human umbilical cord mesenchymal stem cells and promotes adhesion to injured endothelium. [ABSTRACT FROM AUTHOR]

Objective To observe the effects of resveratrol (RSV) on proliferation, migration and tube formation of human umbilical vein endothelial cells (HUVECs) in the context of high glucose. Methods Well-cultured HUVECs in vitro were randomly divided into six groups: blank group, mannitol 30 mmol/L group, model group, low-dose, mid-dose and high-dose RSV groups. The model group was induced by using 30 mmol/L D-glucose. The low-dose, mid-dose and high-dose RSV groups were established through intervention by administering 20 µmol/L, 40 µmol/L, 60 µmol/L RSV respectively for 24 hours. Cell proliferation, migration and tube formation were detected by using Cell Counting Kit-8 (CCK-8), Transwell chamber, wound healing and Matrigel assay respectively. Results The cell proliferation rate, migration number, wound healing rate and lumen branch number in model group were significantly higher than those in blank group and mannitol group (P < 0.05). Compared with model group, after intervention with RSV, the ability of cell proliferation, migration and tube formation were significantly decreased. The cell proliferation rate, migration number, wound healing rate and lumen branch number were significantly decreased in a dose-dependent manner (P < 0.05). When RSV concentration was 60 µmol/L, the proliferation rate, migration number, wound healing rate and lumen branch number were significantly lower than those in model group, blank group and mannitol group. The differences were statistically significant (P < 0.05). Conclusion RSV could inhibit the proliferation, migration and lumen formation of HUVEC cells in high glucose conditions, suggesting that it could protect HUVEC cells from injury induced by high glucose and inhibit pathological angiogenesis. [ABSTRACT FROM AUTHOR]

To investigate the value of ultrasonography in the diagnosis of persistent right umbilical vein (PRUV) with malformation and its prognostic significance for fetus. A total of 6258 pregnant women were collected from our hospital during January 2014 to January 2020. Prenatal evaluation with echocardiography was performed on all fetuses, and further diagnosis was made in fetuses with PRUV. Detailed fetal echocardiographic anatomic scans were performed in all PRUV cases to determine the presence of additional malformations. Hospitalization of pregnant women and their fetuses was recorded in detail in the system of maternal cases delivered in our hospital. The PRUV fetuses that were not delivered in our hospital were followed up by telephone to understand the condition of the fetuses at birth. All 26 PRUV fetuses were followed up by telephone for at least 12 months to understand the prognosis of the fetuses. PRUV ultrasound showed that the umbilical vein ran laterally and to the right side of the gallbladder, and may fuse with the right portal vein running toward the stomach (intrahepatic type), or may drain into the right atrium, inferior part of the inferior vena cava, or iliac vein (extrahepatic type). In the intrahepatic variant, the umbilical vein fuses with the right portal vein at the venous sinus, and placental blood continues to flow into the venous duct and eventually into the inferior vena cava. A total of 26 fetuses with PRUV were found in 6258 pregnant women with regular antenatal examination, the incidence of PRUV was 0.42%(26/6258), of which the intrahepatic type was 0.39%(24/6258) and the extrahepatic type was 0.03% (2/6258). There were 16 (61.54%) cases were PRUV simplex fetuses (except PRUV without other malformations), in which 1 case was delivered by caesarean section due to fetal weight, and the post-partum fetus was healthy. All the other fetuses were delivered naturally and the postpartum fetuses were healthy. There were 10 (38.46%) cases of non-simple PRUV fetuses (except PRUV with other malformations), including 8 cases of intrahepatic PRUV and 2 cases of extrahepatic PRUV. In 8 cases of PRUV of non-simple intrahepatic type, the fetuses with tetralogy of Fallot and single umbilical artery were surgically treated after birth, and the prognosis was poor and they died of infective endocarditis at the age of 1 year. Atrial septal defect closed spontaneously after birth and the fetus was healthy. The prognosis of the other fetuses was good after the operation. 2 cases of non-simple extrahepatic PRUV were combined with acromitis and transposition of the great artery, 1 case died intrauterine and the other died of heart failure 1 week after cesarean section. Detailed prenatal ultrasound may be used to confirm PRUV and its possible concomitant deformities. The prognosis of PRUV fetuses is good with simple PRUV fetuses, and the prognosis of PRUV fetuses with non-simple PRUV fetuses depends on the type and severity of the associated malformations, and the prognosis of PRUV fetuses with non-simple extrahepatic PRUV is poor and the mortality rate is high. [ABSTRACT FROM AUTHOR]

Objective: To investigate the influencing factors of the effect of dydrogesterone in the treatment of early threatened abortion, and follow up the pregnancy outcome of patients with continued pregnancy. Methods: 300 patients with early threatened abortion who were admitted to our hospital from January 2017 to January 2019 were selected. All patients were given the first dose of dydrogesterone 40 mg/time orally, then changed to 30 mg/time, twice a day. They were divided into effective group and ineffective group according to whether the treatment was effective or not, basic clinical dataes of the two groups were collected. Multivariate Logistic regression was used to analyze the influencing factors of the effect of dydrogesterone on early threatened abortion, and the pregnancy outcome was followed up. Results: Among the 300 patients, 245 cases (81.67%) were effective, and 55 cases (18.33%) were ineffective. Univariate analysis showed that compared with the ineffective group, the age, gestational times, abortion times, birth times and anti-endometrial antibody(EMAb) positive rate in the effective group were lower, and the serum levels of β-human chorionic gonadotropin (β-HCG), progesterone (P) and estradiol (E2) were higher, and the differences were statistically significant (P＜0.05). Multivariate Logistic regression analysis showed that: Age (older), gestational times (more), birth times (more), abortion times (more) and EMAb positive were the risk factors affecting the effect of dydrogesterone treatment (P＜0.05). Serum β-HCG (higher), P (higher) and E2 (higher) were the protective factors affecting the effect of dydrogesterone treatment (P＜0.05). Follow-up results showed that the average gestational age of the 245 patients with continued pregnancy was (39.43± 1.06) weeks. The maternal outcomes were as follows: 6 cases had postpartum hemorrhage, and 17 cases had postpartum placental adhesion. Neonatal outcome: Apgar score was (9.43 ± 0.20) score, preterm delivery occurred in 2 cases, malformation occurred in 1 case, and right umbilical vein was permanent in 1 case. Conclusions: Age, pregnancies times, abortion times, EMAB positive, serum β-HCG, P and E2 are the influencing factors for the efficacy of dydrogesterone in the treatment of early threatened abortion, whether the treatment of Early Threatened Abortion with didroxyprogesterone can increase the risk of adverse maternal and neonatal outcomes remains to be further studied. [ABSTRACT FROM AUTHOR]

BACKGROUND: In recent years, acellular decalcified bone matrix (ADBM) exhibits tremendous potential and application prospects in bone defect repair due to its favorable biocompatibility and biomechanics. Erythropoietin (EPO) can promote the formation of local blood vessels and thus indirectly regulate bone repair owing to crucial role in angiogenesis of bone repair. OBJECTIVE: To investigate the effects of acellular decalcified bone matrix/erythropoietin (ADBM-EPO) hydrogel on osteogenesis and angiogenesis. METHODS: ADBM hydrogel and ADBM-EPO hydrogel were constructed. Human bone marrow mesenchymal stem cells and human umbilical vein endothelial cells were respectively seeded on the two hydrogels, and the conventionally cultured cells were used as the control group. The effects on the migration ability of two kinds of cells were detected through cell transmembrane invasion and cell scratch migration experiments. The effects of the two hydrogels on osteogenic differentiation of bone marrow mesenchymal stem cells were determined by alkaline phosphatase and alizarin red staining. RESULTS AND CONCLUSION: (1) Compared with the control group, ADBM hydrogel and ADBM-EPO hydrogel could promote the migration of bone marrow mesenchymal stem cells or umbilical vein endothelial cells. Moreover, the ADBM-EPO hydrogel had better migration ability than that of ADBM hydrogel. (2) Compared with the control group, both ADBM and ADBM-EPO hydrogels could reduce the scratch distance of human bone marrow mesenchymal stem cells or human umbilical vein endothelial cells. Of them, ADBM-EPO hydrogel was more effective than ADBM hydrogel. (3) Compared with the control group, both ADBM and ADBM-EPO hydrogels could increase the alkaline phosphatase activity and the number of calcium nodules in bone marrow mesenchymal stem cells. Moreover, the ADBM-EPO hydrogel had better ability than that of ADBM hydrogel. (4) The above experimental results showed that the ADBM-EPO hydrogel had a bidirectional role in promoting osteogenesis and angiogenesis. [ABSTRACT FROM AUTHOR]

BACKGROUND: Tissue-engineered bone provides a new direction for the repair of large bone defects, but the survival of tissue-engineered bone grafts in vivo can be guaranteed only if the capillary network is formed in the early stage. Therefore, vascularization of early tissue-engineered bone is the key to its clinical application. OBJECTIVE: To explore the effect of bone marrow mesenchymal stem cells and human umbilical vein endothelial cells combined with hydroxyapatite-tricalcium phosphate scaffolds on early angiogenesis in skull defect repair in rats. METHODS: (1) The hydroxyapatite-tricalcium phosphate scaffold was divided into four groups: Group A was added with DMEM culture medium and extracellular matrix culture medium with volume ratio of 1:1. Group B was added with bone marrow mesenchymal stem cells suspension and human umbilical vein endothelial cells suspension with a volume ratio of 1:1. Group C was cultured with DMEM culture medium and human umbilical vein endothelial cells suspension with a volume ratio of 1:1. Group D was cultured with bone marrow mesenchymal stem cells suspension and extracellular matrix medium with a volume ratio of 1:1 for 21 days for in vivo implantation experiment. (2) Bone defects with a diameter of 1 cm were made in the skull of adult SD rats, and materials of groups A, B, C and D were implanted respectively. Skull micro-CT and skull scaffold complex gross, histomorphology, CD31/CD34 immunohistochemical staining, CD31/CD34 molecular content, and vascular endothelial growth factor A protein were detected respectively 4, 8 and 12 weeks after the operation. Animal experiment was approved by the Animal Ethics Committee of Southwest Medical University. RESULTS AND CONCLUSION: (1) Micro-CT showed that 8 weeks after operation, the mass of new bone in group B was higher than that in the other three groups, and the mass of new bone in groups C and D was higher than that in group A. At 12 weeks after surgery, the new bone mass was from high to low: group B>group C>group D>group A. (2) Gross observation showed that the bone crawling area on the scaffold of group B was higher than that of the other three groups, and that of groups C and D was higher than that of group A. At the same time point, the amount of bloody exudate was from most to least: group B>group C>group D>group A. (3) Histological observation showed that at 4 weeks after the operation, the bone regeneration amount from high to low was: group B>group C>group D>group A. At other time points, the bone regeneration amount from high to low was: group B>group D>group C>group A. (4) Immunohistochemical staining showed that at the same time point, the microvascular density of CD31/CD34 was from high to low successively: group B>group C>group D>group A. Except for groups C and D, there was no significant difference (P > 0.05), and the difference between the other groups was significant (P < 0.05). (5) Western blot assay showed that at the same time point, the protein expression of vascular endothelial growth factor A was in descending order from high to low: group B>group C>group D >group A, except for no significant difference between groups C and D (P > 0.05), and the difference between the other groups was significant (P < 0.05). (6) The results showed that bone marrow mesenchymal stem cells and human umbilical vein endothelial cells combined with hydroxyapatite-tricalcium phosphate scaffold materials had strong early vascularization ability in repairing skull defects in rats. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Glial maturation factor-gamma (GMFG) is one of the members of the ADF/cofilin superfamily protein in the process of cytoskeleton remodeling. It can regulate the cell movement by regulating actin-mediated cytoskeleton reorganization. The authors previously found that the high expression of GMFG is associated with the clinicopathological features of colorectal cancer patients, but the specific upstream and downstream mechanisms need to be explored.OBJECTIVE: To study the effects of GMFG on cytoskeleton and LoVo cell proliferation.METHODS: (1) Human umbilical vein endothelial cells were inoculated in a laser confocal dish. After the cells grew stably, the correlation between the expression of GMFG and the expression of cytoskeletal protein F-actin was observed by immunofluorescence staining. Colchicine inhibited mitosis. The cells were divided into control group, 0.5 mg/L colchicine group and 1.0 mg/L colchicine group. The cell cycle was observed by flow cytometry and GMFG protein expression was observed by western blot assay. (2) Human colorectal cancer LoVo cells were inoculated in a laser confocal dish. After the cells grew stably, the correlation between GMFG expression and cell cycle was observed by immunofluorescence staining. Afterwards, siRNA was used to interfere the expression of GMFG in LoVo cells. The LoVo cells were divided into blank control group, empty transfer group and siRNA-GMFG group. The cell proliferation rate was detected by Edu assay. RESULTS AND CONCLUSION: (1) In human umbilical vein endothelial cells, the expression of GMFG was associated with the cytoskeletal motion of human umbilical vein endothelial cells, and the expression of GMFG increased when the cytoskeleton retracted. After colchicine inhibited the mitosis of human umbilical vein endothelial cells, the proportion of cells in G2/M phase increased and the expression of GMFG protein decreased with the increase of colchicine dosage. (2) In LoVo cells, the expression intensity of GMFG was associated with mitosis, and the expression of GMFG was enhanced in the middle and late stages of cell mitosis. (3) After siRNA interference with GMFG in LoVo cells, the cell proliferation rate was decreased. (4) Results verify that interference with GMFG can inhibit the proliferation rate of LoVo cells of human colorectal cancer, and there is a certain correlation between cytoskeletal motion and GMFG expression. [ABSTRACT FROM AUTHOR]

BACKGROUND: Vascular injury is a common complication after balloon dilatation. The development of umbilical cord mesenchymal stem cells (UC-MSCs) provides a new method for treating vascular injury. OBJECTIVE: To investigate the mechanism underlying the repair of damaged blood vessels by human UC-MSCs (hUC-MSCs) transfected with interleukin-8RA/B (IL-8RA/B) adenovirus. METHODS: hUC-MSCs and human umbilical vein endothelial cells (hUVECs) were collected and transfected with adenovirus vectors containing human IL-8RA and/or IL-8RB cDNAs and green fluorescent protein. A rat model of carotid artery injury was established. Sprague-Dawley rats were randomly divided into four groups: IL-8RA/B-hUCMSCs group, Il-8ra/B-hUVECs group, Null-hUCMSCs group, and control group, followed by injection of 0.5×106 corresponding cells (500 μL) and same volume of normal saline via the tail vein respectively at 1, 3, and 5 hours post-surgery. After 30 minutes of injection, the carotid artery was taken and the expression of green fluorescent protein was observed. After 24 hours, the serum levels of inflammatory and anti-inflammatory factors were measured by ELISA; and the infiltration of neutrophil cells and mononuclear macrophages was observed by immunohistochemistry. After 14 days, Evans blue staining was used to observe vascular endothelialization and fibrosis. After 28 days, the neointimal hyperplasia was observed by hematoxylin-eosin staining. RESULTS AND CONCLUSION: (1) After 30 minutes of IL-8RA/B-hUC-MSCs infusion, the expression of green fluorescent protein was observed in the injured vascular intima, and the fluorescence expression was higher than that of the other three groups. (2) After 24 hours of IL-8RA/B-hUC-MSCs infusion, the expression of inflammatory factors in the serum was significantly lower than that of the other three groups, while the expression of anti-inflammatory factor interleukin-10 was higher than that of the other three groups (P < 0.05). In addition, inflammatory cell infiltration in the IL-8RA/B-hUC-MSCs group decreased significantly. (3) hUC-MSCs overexpressing interleukin-8 receptor promoted re-endothelialization of injured vessels and reduced vascular fibrosis after 14 days of infusion. (4) IL-8RA/B-hUC-MSCs reduced vascular neointimal hyperplasia after 28 days of infusion. (5) Interleukin-8 receptor enhances the targeted homing ability of hUC-MSCs, allowing MSCs to migrate to the site of vascular injury, inhibit inflammation, reduce neointimal hyperplasia, and promote vascular repair. [ABSTRACT FROM AUTHOR]

BACKGROUND: In the research of tissue engineering, there are inevitably various kinds of microorganisms attached to animal tissues, and asepsis is a basic requirement of clinical application of tissue engineering materials. OBJECTIVE: To investigate the effect of 75% ethanol sterilization on the properties and biocompatibility of bovine pericardium.METHODS: Bovine pericardial tissue was sterilized with sterile PBS(control group), PBS containing 1% antibiotic(penicillin/streptomycin/amphotericin B solution), chlorhexidine and 75% ethanol. LB solid medium was used to evaluate the bactericidal effect of four methods. VB staining was used to evaluate the effect of four sterilization treatments on the tissue structure of bovine pericardium. The cytotoxicity of four sterilized extracts was determined by the CCK-8 assay. The bovine pericardium was sterilized with 75% ethanol and then used to make acellular scaffold, which was co-cultured with human umbilical vein endothelial cells to observe the effect of cell adhesion and endothelialization. RESULTS AND CONCLUSION:(1) The bovine pericardium treated with 75% ethanol and chlorhexidine for 24 hours met the requirements of complete sterilization, and significant colony formation was observed in 1% antibiotic-treated and control groups.(2) VB staining revealed that the collagen fibers of bovine pericardium treated with 75% ethanol, chlorhexidine and 1% antibiotic were arranged in wavy pattern, with compact structure, less elastic fiber content but clear structure.(3) Bovine pericardium treated with 75% ethanol did not affect the proliferation activity of L929 cells, and the cell survival rate within 1-3 days was more than 100%. Chlorhexidine-sterilized bovine pericardium had strong cytotoxicity, leading to cell death.(4) Human umbilical vein endothelial cells grew and adhered normally on the surface of acellular scaffold. During the 20-day implantation period, the highest number of cells adhering to acellular scaffold appeared on days 8-12. These results suggest that 75% ethanol could effectively eliminate all microorganisms attached to the bovine pericardium without affecting the histological integrity and biocompatibility. [ABSTRACT FROM AUTHOR]

BACKGROUND: Cells cannot survive in the ares 200 μm away from nutrients in vitro. Vascular network construction is crucial for thick tissue and organ regeneration in tissue engineering. Coxial cell printing provides a new wsy to construct vascular-like channels in vitro. OBJECTIVE: To optimize the coaxial cell printing performance of bioink and to build the tissue-engineered scaffolds with vascular-like structure. METHODS: The aseptic sodium alginate solution was prepared by intennittent pasteurization and then frozen. Freeze-dried powder of aseptic silk fibroin was prepared from degummed silk and sealed. The thawed sodium alginate solution was added to the silk fibroin protein freeze-dried powder and human umbilical vein endothelial cells were added to prepare the bioink. The outer axis of the biological three-dimensional printer was connected with the bioink, and the inner axis was connected with the crosslinking agent. The scaffolds were prepared by coaxial printing, and perfomed by optical coherence tomography, scanning electron microscopy observation and tensile test. Coaxial scaffolds were made by freeze-preserved sodium alginate solution for 7 days with human umbilical vein endothelial cells. coxial scaffolds were also made by freeze-dried sodium alginate solution for 7 days with human umbilical vein endothelial cells and silk fibroin protein sealed for 6 months. The cell survival rate was detected by dead and alive staining after 24 hours of culture in vitro. Vascular-like scaffolds with series and parallel structures were designed and printed. The cell proliferation was detected after 1, 3, 7, 10, and 14 days of culture. RESULTS AND CONCLUSIONS: (1) The optical coherence tomography showed that the maximum printing height of the bioink was 9 layers and the overall thickness was about 4.4 mm. Scanning electron microscopy showed that the outer wall of hollow fiber-filament of vascular-like scaffolds presented irregular strip-shaped crimp with micron-scale internal connected pore structure, while the inner wall of hollow fiber-filament had denser pore structure. (2) The elastic modulus of silk protein freeze-dried scaffold was higher than that of sodium alginate solution (P < 0.05). (3) The cell survival rate of scaffolds treated with sodium alginate solution for 7 days wss (86.7士3.4)%,and that of scaffolds treated with silk protein freeze-dried powder for 7 days was (98.1士1.2)%, indicating that the sodium alginate solution freeze-­preserved for 7 days was free of bscteria and the shelf-life of silk protein could be up to 6 months. (4) The proliferation activity of cells cultured with parallel structure for 7, 10, and 14 days was higher than that with series structure (P < 0.05). (5) These results imply that the scaffolds have good biocompatibility and mechanical properties. [ABSTRACT FROM AUTHOR]

BACKGROUND: The research on neovascularization in diabetic retinopathy is mostly limited to vascular endothelial growth factor, but 6-phosphofructokinase-2/fructose-2,6-diphosphatase (PFKFB3) also plays a certain role. OBJECTIVE: To investigate the effect of PFKFB3-siRNA on human umbilical vein endothelial cells (HUVECs) in high glucose environment. METHODS: HUVECs were divided into four groups: nonnal glucose control group (5.5 mmol/L glucose), nonnal glucose+PFKFB3-siRNA group (5.5 mmol/L glucose+PFKFB3-siRNA), high glucose group {30 mmol/L glucose), high glucose+PFKFB3-siRNA group (30mmolll glucose+PFKFB3-siRNA). Western blot assay was used to detect the silencing effect of PFKFB3 expression. PFKFB3 with optimal silencing effect was selected for subsequent experiments. The tubule formation was detected by in vitro tubule formation assay. The expression of PFKFB3 mRNA was detected by real-time fluorescent quantitative PCR. The expression of PFKFB3 and AKT protein was detected by western blot. RESULTS AND CONCLUSION: PFKFB3-siRNA significantly inhibited the expression of PFKFB3 (P < 0.01). Compared with the normal glucose control group, the total length of tube formation was increased in the nonnal glucose+PFKFB3-siRNA group (P < 0.05), and was significantly decreased in the high glucose group (P < 0.01 ). There was no significant change in the total length of tube formation between normal glucose control group and high glucose+PFKFB3-siRNA group (P > 0.05). Compared with the high glucose group, the tube formation ability of the high glucose+PFKFB3-siRNA group was significantly increased (P < 0.05). Compared with the normal glucose control group, the mRNA and protein expression of PFKFB3 in the high glucose group were significantly increased (both P < O .Q1 ). Compared with the high glucose group, the expression of PFKFB3 protein in the high glucose+PFKFB3-siRNA group was decreased (P < 0.05}. Compared with the normal glucose control group, the ratio of p-AKT/AKT in the normal glucose+PFKFB3-siRNA group and the high glucose group was decreased (both P < 0.01}, while there was no significant difference in the ratio p-AKT/AKT protein between the high glucose group+PFKFB3-siRNA group and the normal glucose control group (P > 0.05). Compared with the high glucose group, the ratio of p-AKT/AKT protein in the high glucose+PFKFB3-si RNA group was increased {P < 0.01 ). To conclude, siRNA silencing of PFKFB3 gene expression can inhibit the expression of PFKFB3 and improve tube formation in HUVECs. The mechanism may be related to the down-regulation of AKT expression. [ABSTRACT FROM AUTHOR]

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BACKGROUND: Our previous study demonstrated that bone marrow mesenchymal stem cells (MSCs) presented with a low survival rate and newly formed vascular-like structures was sparsely distributed in the local infarct tissues after cell transplantation, which certainly impaired the therapeutic efficacy. Long non-coding RNA-H19 (lncRNA-H19) has been confirmed to be associated with MSCs differentiation and mediate vascularization. OBJECTIVE: To observe the influence of lncRNA-H19 on the survival and vascularization potential of MSCs in vitro and to explore the possible mechanism. METHODS: MSCs were obtained and cultured in vitro. Cells were divided into five groups: MSCs+H19, MSCs+H19 negative control (MSCs+H19 NC), MSCs+si-H19, MSCs+si-H19 negative control (MSCs+si-H19 NC) and MSCs groups. MSCs+H19 and MSCs+H19 NC groups were transfected with lncRNA-H19 and lncRNA-H19 scramble RNA respectively, while MSCs+siH19 and MSCs+si-H19 NC groups were transfected with lncRNA-H19 siRNA and lncRNA-H19 siRNA scramble respectively. Cells were cultured under hypoxic-ischemic condition (serum-free medium, 1% O2) for 24 hours. Then, cell proliferation and apoptosis were evaluated using MTS and TUNEL, respectively. Cell supernatant from each experimental group was further co-cultured with human umbilical vein endothelial cells to induce vascularization. The expression of vascular endothelial growth factor A (VEGFA) was thereafter detected using western blot assay. RESULTS AND CONCLUSION: Compared with MSCs+H19 NC and MSCs groups, MSCs+H19 group presented with significantly higher proliferation rate, lower apoptosis percentage and a larger number of vascular branches on matrigel (P < 0.01). There was a significantly higher expression of VEGFA in the MSCs+H19 group than MSCs+H19 NC and MSCs groups. Compared with the MSCs and MSCs+si-H19 NC groups, MSCs+H19 group presented with significantly lower proliferation rate, higher apoptosis percentage and a less number of vascular branches on matrigel (P < 0.01). In addition, VEGFA expression was distinctly downregulated in the MSCs+si-H19 group in comparison with the MSCs+si-H19 NC and MSCs groups. These findings indicate that lncRNA-H19 effectively promotes MSCs survival and vascularization under hypoxic-ischemic condition in vitro, and this effect may be associated with the upregulation of VEGFA. [ABSTRACT FROM AUTHOR]

BACKGROUND: How to promote the early vascularization of large tissue-engineered bone has become the hotspot of current research. Cell co-culture and the addition of bioactive factors to promote angiogenesis are very good methods to promote early vascularization. OBJECTIVE: To explore the ability of angiogenesis by co-transplantation of bone marrow mesenchymal stem cells (BMSCs) and human umbilical vein endothelial cells (HUVECs) which were transfected with vascular endothelial growth factor 165 (VEGF165) gene in vivo, to move forward a single step to offer theoretical basis and experimental basis to build vascularized tissue-engineered bone which can be used to repair large segmental bone defects. METHODS: We built an ischemic skin flap with 4 cm×1.5 cm in the back of Sprague-Dawley rats, and then BMSCs+VEGF165-transfected HUVECs (group A), VEGF165-transfected HUVECs (group B), BMSCs+non-transfected HUVECs (group C), non-transfected HUVECs (group D), DMEM (group E) were respectively transplanted. ELISA method was used to detect peripheral blood VEGF level. Histologically, survival and microvessel density of the flap were observed. RESULTS AND CONCLUSION: (1) The flap survival quality of group A was better than that in the other groups. VEGF exhibited high expression continuously high expression at 2, 4, 7, 14 days after transplantation, and reached the peak at 7 days, but the expression level at 14 days was obviously lower than that at 2 days postoperatively. The VEGF level of group always exceeded that in group B at different time points (P < 0.05). The flap survival rate and microvessel density of group A was significantly higher than that in the other groups at 11 days postoperatively (both P < 0.05). In summary, co-transplantation of BMSCs and VEGF165-transfected HUVECs can promote survival of an ischemic flap in vivo through pro-angiogenic actions. [ABSTRACT FROM AUTHOR]

BACKGROUND: Vascularized bone tissue engineering is a hotspot of current research and early vascularization of tissue-engineered bone also becomes an urgent problem to be solved. Addition of bioactive factors and cell co-culture method both contribute to promoting the early vascularization. OBJECTIVE: To investigate the pro-angiogenic effect of human umbilical vein endothelial cells (HUVECs) transfected with vascular endothelial growth factor 165 (VEGF165) co-cultured with bone marrow mesenchymal stem cells (BMSCs). METHODS: HUVECs were transfected with VEGF165 and then co-cultured with BMSCs which were purified from mouse femoral bone marrow. There were six groups in this experiment: (1) AdVEGF165-HUVECs+BMSCs, (2) AdVEGF165-HUVECs, (3) AdGFP-HUVECs+BMSCs, (4) AdGFP-HUVECs, (5) HUVECs+BMSCs, and (6) HUVECs (blank control). Cell counting kit-8 detection was applied to analyze the proliferative ability of HUVECs. The abilities of HUVECs migration and vascularization were then detected by crystal violet staining and matrigel determination, respectively. RESULTS AND CONCLUSION: Compared with the blank control group, the proliferation of HUVECs was significantly increased in the other groups except for AdGFP-HUVECs group (P < 0.05). Compared with the blank control group, the migration and vascularization abilities of HUVECs were significantly stronger in the group of AdVEGF-HUVECs+BMSCs (P < 0.05). To conclude, the co-culture of HUVECs transfected with VEGF165 and BMSCs could promote early vascularization effectively. [ABSTRACT FROM AUTHOR]

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Objective: To explore the proangiogenic activities of five main components from Danhong injection (DHI) absorbed in blood. Metiiods: A in vitro culture system of human umbilical vein endothelial cells (HUVEC) and a model ofchicken embryo chorioallantoic membrane (CAM) were used in this study. Cells or chicken embryos were randomly divided into control (Con) group, DHI group, hydroxysafflor yellow A (HSYA) group, salvianolic acid B (Sal B) group, Tanshinol (Tan) group, protocatechuic aldehyde (Pra) group and Rosmarinic acid (RosA) group. Results: In comparison with Con group, 10% (V /V )DHI and its five main components at corresponding concentrations could significantly promote HUVEC proliferation (P<0.01) and the expression of vascular endothelial growth factor A (VEGF-A), basic fibroblast growth Factor (bFGF) and hepatocyte growth factor (HGF) in HUVEC (P<0.05, P<0.01). Also, 50 % (V /V )DHI and these components at corresponding concentrations were able to boost the blood vessel density on CAM to different extent. Consistently, HSYA and Tan showed better proangiogenic action in both models. Conclusions: All the five main components from Danhong injection (DHI) absorbed in blood promote angiogenesis and HSYA and Tan have stronger proangiogenic activities than the others. [ABSTRACT FROM AUTHOR]

Objective To study high glucose induced expressiont of endothelial adhesion molecule inhibited by propofol in umbilical vein endothelial cells, and to investigate its mechanism. Methods Human peripheral mononuclear cells were prepared with Histopaque-1077 solution. Nitric oxide (NO) production was measured with an assay kit. Vascular cell adhesion molecule 1 (VCAM-1) expression, endothelial nitric oxide synthase (eNOS) total protein, dimer and monomer expression, eNOS phosphorylation and caveolin-1 were measured by Western blot. Results High glucose induced VCAM-1 expression, increased mononuclear-endothelial adhesion and reduced NO production. Propofol improved NO level, and inhibited VCAM-1 expression and mononuclear-endothelial adhesion. The protective effect of propofol would be blocked by an eNOS inhibitor of L-NAME. Propofol increased high glucose-mediated eNOS-Ser1177 phosphrylation and dimmer/monomer ratio, and attenuated high glucose-induced eNOS-Thr495 phosphrylation and caveolin-1 expression. Conclusions Propofol improved high glucose mediated eNOS phosphrylation, dimer/monomer ratio and caveolin-1 expression, so that NO production was improved and VCAM-1 expression and mononuclear-endothelial interaction were inhibited. [ABSTRACT FROM AUTHOR]

Objective To investigate the protective effects of folic acid on the oxidative damage that ox-LDL (oxidized low-density lipoprotein receptor 1) render to human umbilical vein endothelial cells (HUVEC). Methods HUVECs were injured by ox-LDL (120 mg/L) for 24 h while they were incubated with various concentration of folic acid (0, 15, 60, 150, 225, 300, 375 nmol/L). Then HUVECs were cultured in media contains same concentration of folic acid but without ox-LDL for 72 hours. Finally, HUVECs were harvested after 24, 48, 72 and 96 h. The morphological changes were observed using inverted microscope and cell viability were examined by MTT. Results Various concentrations of folic acid (0,15, 50, 100, 200 and 500 nmol/L) has no obvious promotion or inhibition effect in growth of normal HUVEC (P>0.05). However, compared with the ox-FA-def group, 150, 225, 300 and 375 nmol/L of folic acid promoted proliferation of HUVECs with 96 and 120 hours of incubations (P < 0.05). Folic acid of 60, 150, 225, 300 and 375 nmol/L promoted the proliferation of HUVECs with 72 h and 96 hours of incubation (P < 0.05). Conclusion High dose folic acid can reduce the ox-LDL oxidative damage on HUVEC in a concentration dependent manner. [ABSTRACT FROM AUTHOR]