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Objective To observe the cell viability, pyroptosis, inflammation and oxidative stress response of the preeclampsia (Preeclampsia, PE) model cells constructed using the human chorionic trophoblast cell line HTR-8/SVneo with low expression of microRNA-148a (miR-148a). Methods Human chorionic trophoblast cell line HTR-8/SVneo in the logarithmic growth phase were selected and divided into groups A, B, C, and D. Cells in the group A were transfected with miR-148a inhibitor (inhibiting miR-148a expression) for 24 h, followed by the addition of 100 ng/L LPS for 24 h (establishing a PE model cell); cells in the group B were transfected with NC inhibitor (blank control) and cultured for 24 h, followed by the addition of 100 ng/L LPS for 24 h; cells in the group C were cultured with 100 ng/L LPS for 24 h; cells in the group D were not treated. At 48 h of culture, qRT-PCR was used to detect miR-148a in cells of each group; CCK-8 was used to detect cell viability in each group; TUNEL method was used to calculate the apoptosis rate in each group; Western blotting was used to detect the apoptosis-related proteins Caspase-1, GSDMD, and NLRP3 in each group; ELISA was used to detect inflammatory factors (tumor necrosis factor-a [TNF-a], interleukin-1B [IL-1B], IL-6) and oxidative stress indicators (glutathione peroxidase [GSH], superoxide dismutase [SOD], and malondialdehyde [MDA]) in the supernatant of each group. Results Compared with the group D, the relative expression level of miR-148a was higher, and the OD values were lower at 24, 48, and 72 h of culture, the apoptosis rate was higher, and the relative expression levels of Caspase-1, GSDMD, and NLRP3 proteins in cells were higher in the group C (all P<0.05). Compared with the group B, the relative expression level of miR-148a was lower, and the OD values were higher at 24, 48, and 72 h of culture, the apoptosis rate was lower, and the relative expression levels of Caspase-1, GSDMD, and NLRP3 proteins in cells were low- er in the group A (all P<0.05). Compared with the group D, the levels of TNF-a, IL-1B, and IL-6 in the cell supernatant increased, the expression levels of GSH and SOD in cells were lower, while the expression of MDA increased in the group C (all P<0.05). Compared with the group B, the levels of TNF-a, IL-1B, and IL-6 in the cell supernatant were lower, the expression levels of GSH and SOD increased, and the expression of MDA decreased in the group A (all P<0.05). Conclusions The cell viability of the PE model cells constructed using HTR-8/SVneo with low expression of miR-148a is high, while the degree of pyroptosis, inflammatory response and oxidative stress response are low. MiR-148a may be one of the therapeutic targets of PE. [ABSTRACT FROM AUTHOR]

Objective To investigate the influence of pterostilbene on oxidative stress and inflammatory reaction in diabetic cataract (DC) rats by regulating AMP-activated protein kinase (AMPK) /silent information regulator 1 (SIRT1) / peroxisome proliferator activated receptor γ coactivator-1α (PGC-1α) signaling pathway. Methods Sixty-four SD rats were injected intraperitoneally with streptozotocin to establish the DC models, and they were randomly divided into the model group, low-dose pterostilbene group, medium-dose pterostilbene group, high-dose pterostilbene group, and high-dose pterostilbene +AMPK inhibitor (Dorsomorphin) group, with 12 DC model rats in each group; another 12 SD normal rats were injected intraperitoneally with an equal volume of citrate buffer as the control group. Rats in the low-dose, medium-dose and high-dose perostilbene groups were given 2, 4 and 8 mg/mL perostilbene solution by gavage (10 mL/kg), and 0. 9% sodium chloride solution by tail vein injection (10 mL/kg) . The rats in the high-dose perostilbene+Dorsomorphin group were given 8 mg/mL perostilbene solution by gavage (10 mL/kg), and 0. 02 mg/mL Dorsomorphin solution by tail vein injection (10 mL/kg) . Rats in both the model group and the control group were given 0. 9% sodium chloride solution by gavage (10 mL/kg), and 0. 9% sodium chloride solution by tail vein injection (10 mL/kg) . The rats in each group were given drug intervention once a day in the above manner for 14 days. After corresponding intervention in each group, the fasting blood glucose of rats was measured; the lens opacity was observed and scored by slit lamp; hematoxylin-eosin staining was used to detect the changes of lens tissue structure of rats; the colorimetry was used to measure the malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels in the lens tissues of rats; the enzyme-linked immunosorbent assay was used to measure the serum interleukin (IL) -6, IL-17, and IL-10 levels; Western blotting was used to detect the expression levels of epithelial-mesenchymal transition marker proteins (Vimentin, N-cadherin, and E-cadherin) and AMPK/SIRT1/PGC-1α pathway proteins in lens tissues of rats. Results Compared with the control group, the lens epithelial cells in the model group migrated and aggregated to the lens fibroblasts in the form of sheets and cords; the fasting blood glucose, lens opacity score, serum levels of IL-6 and IL-17, and protein expression levels of MDA, Vimentin and N-cadherin in lens tissues increased significantly (all P<0. 05), the levels of SOD and GSH-Px in lens tissues, serum level of IL-10, and the protein expression levels of p-AMPK/AMPK and SIRT1, PGC-1α and E-cadherin in the lens tissues decreased significantly (all P<0. 05). Compared with the model group, the above-mentioned morphological changes, migration and aggregation of lens epithelial cells in the low-dose, medium-dose and high-dose pterostilbene groups were improved, the fasting blood glucose, lens opacity score, serum levels of IL-6 and IL-17, and protein expression levels of MDA, Vimentin and N-cadherin in lens tissues decreased (all P<0. 05), the levels of SOD and GSH-Px in lens tissue, serum level of IL-10, and the protein expression levels of p-AMPK/AMPK and SIRT1, PGC-1α and E-cadherin in lens tissues increased (all P<0.05), with a dose-dependent manner (P<0. 05) . Compared with the high-dose pterostilbene group, the above-mentioned morphological changes and migration and aggregation of the lens epithelial cells in the high-dose pterostilbene +Dorsomorphin group were aggravated, the fasting blood glucose, lens opacity score, serum levels of IL-6 and IL-17, and protein expression levels of MDA, Vimentin and N-cadherin in lens tissues increased (all P< 0. 05), the levels of SOD and GSH-Px in lens tissues, serum level of IL-10, and the protein expression levels of p-AMPK/ AMPK and SIRT1, PGC-1α and E-cadherin in the lens tissues decreased significantly (all P<0. 05) . Conclusion Pterostilbene can reduce the oxidative stress and inflammatory response in DC rats by activating AMPK/SIRT1/PGC-1α signaling pathway. [ABSTRACT FROM AUTHOR]

Objective To investigate the preventive effect of miR-132 on sevoflurane-induced cognitive dysfunction in newborn mice and its possible mechanism. Methods Sixty-four SPF healthy male 6-day-old C57BL/6 mice were ran‐ domly divided into four groups：normal control group(group A), sevoflurane group(group B), sevoflurane+agomir-NC group(Group C), and sevoflurane+agomir-132 group(Group D), with 16 mice in each group. Except for group A, mice in the other three groups all inhaled 4% sevoflurane continuously for 4 h to induce mouse cognitive dysfunction models. The lateral ventricle of mice in the group C and group D was injected with agomir-NC and agomir-132, respectively, be‐ fore modeling, and mice in the group A and group B with equal volume of normal saline. At 24 h after sevoflurane induc‐ tion, 8 mice in each group were randomly selected to obtain hippocampal tissues. The expression of miR-132 in hippocam‐ pal tissues of mice in each group was detected by qRT-PCR, the expression of HMGB1, Bax and Bcl-2 protein in hippo‐ campal tissues of mice in each group was detected by Western blotting, and the levels of tumor necrosis factor-α(TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and malondialdehyd(MDA)in hippocampus were detected by ELISA. The remaining 8 mice in each group underwent the Morris water maze test to test their neurocognitive function at the sexual maturity stage. Results Compared with group A, the relative expression of miR-132 in the hippocampus of groups B, C, and D all decreased(all P<0. 05)；there was no significant difference in the relative expression of miR-132 in the hippocampus between the group B and group C(P> 0. 05). Compared with group B and group C, the relative expression of miR-132 in the hippocampus of group D increased (P<0. 05). Compared with group A, the escape latency and swimming distance of groups B, C and D increased(all P< 0. 05), and the stay time in the original platform quadrant and the number of times of crossing the original platform position decreased(all P<0. 05)；there was no significant difference in the above indexes between the group B and group C(all P> 0. 05). Compared with group B and group C, the escape latency and swimming distance of group D were shortened(all P< 0. 05), and the stay time in the original platform quadrant and the number of times of crossing the original platform position increased(all P<0. 05). Compared with group A, the expression of HMGB1 protein and the levels of inflammatory factors such as IL-1β, TNF-α, and IL-6 in the hippocampus of groups B, C, and D all increased(all P<0. 05)；there was no sig‐ nificant difference between the group B and group C(all P>0. 05). Compared with group B and group C, the expression of HMGB1 protein and the levels of inflammatory factors such as IL-1β, TNF-α, and IL-6 in the hippocampus of group D de‐ creased(all P<0. 05). Compared with group A, the levels of SOD, GSH-PX and Bcl-2 protein in hippocampus of groups B, C and D decreased(all P<0. 05), while the levels of MDA and Bax protein increased(all P<0. 05)；no significant dif‐ ferences were found in the above indexes between group B and group C(all P>0. 05). Compared with group B and group C, the levels of SOD, GSH-PX and Bcl-2 protein in hippocampus of group D increased(all P<0. 05), while the levels of MDA and Bax protein decreased(all P<0. 05). Conclusion MiR-132 can prevent sevoflurane-induced cognitive dys‐ function in newborn mice. The mechanism may be that miR-132 reduces the release of inflammatory factors, oxidative stress and apoptosis by inhibiting the expression of HMGB1 gene. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of microRNA-146a (miR-146a) on cognitive ability, Th17/Treg distribution and inflammatory factor levels in Alzheimer's disease (AD) rats. Methods Sixty SD rats were randomly di‐ vided into the sham operation group, AD group and miR-146a+AD group, with 20 cases in each group. Rats in the AD group and miR-146a+AD group were injected with Aβ25-35 in the hippocampus to make AD models, while the rats in the sham operation group were only injected with the same amount of normal saline after craniotomy, and sealed with bone wax. The rats in the miR-146a+AD group were then injected with 100 μL of 1×108 PFU/mL of miR-146a agomir through the tail vein. Cognitive ability of rats was evaluated by water maze test, serum Th17/Treg distribution was detected by flow cytometry, and inflammatory factors tumor necrosis factor-α (TNF-α), interleukin (IL) -1β, and IL-6 in hippocampus were detected by ELISA. Results The escape latency from 1 to 4 days after modeling in the AD group was longer than that in the sham operation group, the duration of stay in the target quadrant was shorter and the number of crossing the platform was smaller than those in the sham operation group, and the escape latency in the miR-146a+AD group was shorter than that in the AD group, and the duration of stay in the target quadrant was longer and the number of crossing the plat‐ form was larger than those in the AD group (all P<0. 05) . The ratio of CD4+ IL-17A+ Th17 was lower, and the ratio of CD4+ CD25+ Foxp3+ Treg was higher in the AD group than those in the sham operation group; the ratio of CD4+ IL-17A+ Th17 was higher, and the ratio of CD4+ CD25+ Foxp3+ Treg was lower in the miR-146a+AD group than those of the AD group (all P <0. 05) . The levels of serum IL-1β, IL-6, and TNF-α in the AD group were higher than those in the sham operation group, and the levels of serum IL-1β, IL-6, and TNF-α in the miR-146a+AD group were lower than those in the AD group (all P<0. 05) . Conclusion MiR-146a can improve the cognitive ability of AD rats, regulate Th17/Treg balance, and re‐ duce AD brain inflammation. [ABSTRACT FROM AUTHOR]

Objective To analyze the genes closely related to the pathogenesis of ulcerative colitis (UC), and to screen the active ingredients of Chinese herbal medicine used in the treatment of UC by using bioinformatics method. Methods The data set of UC related gene chip (GSE87466) was obtained from GEO database. The colonic mucosa sam‐ ples in 87 patients with UC and 21 healthy people were included and we screened the differentially expressed genes (DEGs) in the colonic mucosa tissues in patients with UC and normal people. DAVID database was used to analyze gene ontology and signaling pathway enrichment of differentially expressed genes. STRING and Cytoscape were used to analyze protein-protein interaction（PPI）network of DEGs associated with pathogenesis of UC to find the core pathogenic genes. The comparative toxicogenomics database was used to interconnect the pathogenic core genes of UC with the relevant active components of traditional Chinese medicine to obtain active components of traditional Chinese medicine that may be used to treat UC. Results Core genes associated with pathogenesis of UC included interleukin-8 (IL-8), matrix metallo‐ proteinase-9 (MMP-9), epidermal growth factor (EGF)，interleukin-1β (IL1β), chemokine ligand 2 (CCL2), CCL1, in‐ terleukin-10 (IL-10) and IL-2. Further studies found that the active ingredients of Chinese medicine that was used to treat UC included resveratrol，quercetin, curcumin, etc. Conclusions There are 279 DEGs associated with UC, and 8 core genes including IL-8, MMP-9, etc. Resveratrol, quercetin and other 46 kinds of active ingredients of traditional Chi‐ nese medicine are obtained to be used to treat UC. [ABSTRACT FROM AUTHOR]

Objective To observe the inhibitory effect of Buyang Huanwu Decoction on pulmonary fibrosis in rats， and to explore its mechanism through the change of transforming growth factor- β（TGF- β）/Smads pathway. Methods Thirty-six SD rats were randomly divided into three groups with 12 rats in each group. Rats in the model group and intervention group were given bleomycin to establish the pulmonary fibrosis models. After models were established，Buyang Wuhuan Decoction and normal saline were given by intratracheal gavage，once a day，while rats in the control group were injected with normal saline intratracheally，once a day. Rats were executed and their lung tissues were taken out after a week. The pathological changes of lung tissues were observed by HE staining，the scores of alveolar inflammation and pulmonary fibrosis were evaluated after Masson staining，TGF-β mRNA and Smad3 mRNA in the lung tissues were detected by RT-PCR，and TGF- β and p-Smad3 proteins in the lung tissues were detected by Western blotting. Results Com⁃ pared with the control group，a large number of inflammatory cells were seen in the pulmonary alveoli，and proliferation of fibroblasts in the lung tissue，and formation of large-area fibrotic lesions were found in the model group，and the degree of pathological changes in the intervention group was lighter than that in the model group；scores of pulmonary alveolar inflammation and pulmonary fibrosis were higher in the model group than in the control group（both P<0.05)，which were lower in the intervention group than in the model group（both P<0.05)；the levels of TGF- β mRNA and Smad mRNA3 in the lung tissues were higher in the model group than in the control group（both P<0.05)，which were lower in intervention group than in the model group（both P<0. 05)；the levels of TGF-β protein and p-Smad3 protein were higher in the model group than in the control group（P<0. 05)，which were lower in the intervention group than in the model group（both P< 0.05). Conclusion Buyang Huanwu Decoction can delay the progression of pulmonary fibrosis by inhibiting activation of TGF-β/Smads signaling pathway. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of pioglitazone on inflammatory response of THP-1 cells induced by monosodium urate ( MSU) and its mechanism. Methods The THP-1 cells were cultured in vitro. Pioglitazone aud T0070907, an specific inhibitor of peroxisome proliferator-activated receptor- γ (PPAR- γ), were used to treat the MSU-induced THP-1 cells. The cells were divided into three groups and pre-treated with PMA for 24 h, aud then PBS, T0070907, Piog were separately added to the three groups aud treated for 1 h. After that, all the three groups were then divided into two groups. One group was not treated, and the other group was stimulated with MSU for 16 h in the same environment of 37°C aud 5% C02, and then this group were divided into six groups: PBS, 10070907, Piog, MSU, MSU + T0070907 aud MSU + Piog groups. The above cells were labeled with IL-1β antibody, aud then were detected by flow cytometry to research the composition ratio. IL-1β level in the THP- 1 cells were assessed by ELISA. To further investigate the mechanism of Piog, LY294002 was used to block the expression of protein kinase B (AKT). The THP-1 cells were then divided into four groups: PBS, PBS +MSU, PBS +MSU +Piog, aud PBS+ MSU +Piog + LY294002 groups. Then the protein expression of p-AKT, AKT, aud PPAR- γ in THP-1 cells was detected by Western blotting. Results Compared with the other groups, the composition ratio of IL-1[3-labelled positive THP-1 cells in the MSU group aud MSU + T0070907 group increased ( P < 0. 05). Statistically significant difference was found in the levels of IL-1β in the supematants of THP-1 cells in the six groups ( P < 0. 05) . The levels of IL-1β in the MSU group and MSU + T0070907h group were higher than those in the PBS group, T0070907 group and Piog group, while MSU + The Piog group was lower than the MSU group and the MSU +T0070007 group (all P <0.05). Statistically significant differences were found in the relative protein expression levels of p-AKT, AKT and PPAR-γ among the PBS group, PBS + MSU group, PBS + MSU + Piog group, and PBS + MSU + Piog + LY294002 group (all P <0. 05) . Conclusion Pioglitazone inhibits the MSU-induced inflammation in THP-1 cells by activating the PPAR-γ/AKT pathway. [ABSTRACT FROM AUTHOR]

Objective To compare the effects of propofol and sevoflurane on acute kidney injury ( AKI) in infants undergoing pediatric living donor liver transplantation. Methods Eighty infants undergoing pediatric parent liver transplantation under general anesthesia were randomly divided into two groups, with 40 in each. We used the same anesthetic induction drugs，with oral endotracheal intubatton，and mechanically controlled ventilation. Anesthesia maintenance ： in the group sevoflurane (S)，the infants continued to inhale sevoflurane and we maintained end-tidal concentration of 2.5% to 3. 0% ï¼› in the group propofol ( P)，the infants received 1 % propofol intravenously 9-15 mg / ( kg • h) ï¼› the infants in the two groups received intermittent intravenous injection of fentanyl 1-3 jjig/kg, intravenous infusion of atracurium cisbesulfate 0. 12 mg / (kg * h) to maintain muscle relaxation. Central venous blood samples were collected at the immediate incision (T\ )，at 30 min of anhepatic phase ( T2 )，at 3 h of neohepatic phase ( T3 )，at 24 h after surgery ( T4 ) and at 3 d after surgery ( T5 ). The hemodynamic indicators were monitored, and the levels of serum creatinine ( Scr) was detected by colorimetric method to determine whether or not acute kidney injury ( AKI) occurred. The levels of tumor necrosis factor-a (TNF-a)，interleukin -18 (IL-18)，interleukin -10 (IL-10) and neutrophil gelatinase-associated lipocalin ( NGAL) were detected by enzyme-linked immunosorbent assay (ELISA). Results Compared with group P，the incidence of AKI was lower in the group S，the mean arterial pressure fluctuation was smaller, the serum levels of TNF-a, IL-18 and NGAL were lower ( all P bilizes hemodynamic changes and inhibits inflammatory response [ABSTRACT FROM AUTHOR]

Objective To observe the effects of macrophage migration inhibitory factor( MIF) gene silencing on cardiac function in rats with myocardial infarction and to investigate its possible mechanism. Methods Forty clean-grade SD rats were randomly divided into the sham operation group, saline group, Adv-blank vector group, and Adv-siRNA-MIF group, with 10 in each group. AMI model was constructed by ligation of left anterior descending coronary artery. We injected siRNA-MIF recombinant adenovirus vector into the left ventricular free wall of rats in the Adv-siRNA-MIF group, while in the saline group and Adv-blank vector group, rats were given the same amount of physiological saline and blank adenovirus vector. After modeling of 14 d, the heart function of each group was detected by using ultrasound. The morphological changes of myocardial tissues in each group were observed by HE staining. TUNEL method was used to detect the cardiomyocyte apoptosis in each group. Western blotting was used to detect the expression of MIF protein in myocardial tissues of rats in each group. The expression of MIF, MCP-1, IL-1β, IL-6, IL-8 and TNF-α mRNA in the myocardial tissues of rats in each group was detected by real-time fluorescent quantitative PCR. Results Compared with the saline group and Advblank vector group, left ventricular end diastolic diameter and left ventricular end-systolic diameter decreased, the left ventricular ejection fraction increased, the cardiomyocyte injury and apoptotic index of cardiomyocytes decreased, the relative expression levels of MIF protein and mRNA, and the relative expression levels of MCP-1, IL-1β, IL-6, IL-8 and TNF-αmRNA decreased in the Adv-siRNA-MIF group( all P < 0. 05). Conclusion Recombinant adenovirus vector-mediated MIF gene silencing can effectively improve cardiac function in rats with AMI by inhibiting the inflammatory response and thereby reducing myocardial apoptosis. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of emodin on lung tissue inflammation and p38 mitogen-activated protein kinase(p38 MAPK) expression in mice with Streptococcus pneumonia. Methods Thirty-two female BALB/c mice were divided into the control group, pneumonia model group, emodin group, and cefuroxime group with 8 in each. All mice were anesthetized with 5% chloral hydrate 5 ul/g intraperitoneally. After anaesthesia in mice of the pneumonia model group, emodin group, and cefuroxime group, their nasal mucosa was pierced with a sterile needle, and 0. 5 Maxwell unit of bacterial suspension 50 μL was slowly instilled into the rat nasal cavity. The mice in the control group were instilled with 50μL normal saline. Pre-experimentation confirmed that the model was successfully established. Then, the mice in the emodin group were treated with 25 mg/(kg·d) emodin by gavage, the cefuroxime group with 50 mg/(kg·d) cefuroxime, once a day, for 7 days. The mice in the control group and model group were given the same mount of normal saline instead. After the last gavage for 12 h, all the mice were anesthetized with chloral hydrate, the lung tissues of the mice were obtained, the left lung of the mice was used for HE staining, and the pathological manifestations of lung tissues were observed under light microscope. The levels of interleukin-1β(IL-1β), IL-6, and TNF-α in the lung tissues were detected by ELISA. The expression of p38 MAPK mRNA in the lung tissues was detected by PCR. The expression of P38 MAPK protein in the lung tissues was detected by Western blotting. Results In the control group, the alveolar structure was intact, and there was no obvious inflammatory cell infiltration in the alveolar septum. A large number of inflammatory cells infiltrated in the model group, and the inflammatory cell infiltration of the emodin group and the cefuroxime group was between the above two. The levels of IL-1β, IL-6, TNF-α and the expression of p38 MAPK mRNA and protein in the model group were higher than those in control group(all P < 0. 05). The levels of IL-1β, IL-6, and TNF-α in the emodin group and cefuroxime group were lower than those in the model group(all P < 0. 05). The expression of p38 MAPK mRNA and protein in the emodin group was lower than that in model group(both P < 0. 05). Conclusion Emodin can inhibit the pulmonary inflammatory response in mice with Streptococcus pneumonia by inhibiting the expression of p38 MAPK mRNA and protein. [ABSTRACT FROM AUTHOR]

Objective To explore the influence of different pressure of ultrasound-targeted microbubble destruction on the expression of inflammatory factor and vascular endothelial growth factor ( VEGF) in human umbilical vein endothelial cells (HUvE-12 cells). Methods We cultured HUvE-12 cells in the DMEM-F12 medium containing 1 xl07/mL micro­bubbles. HUvE-12 cells were divided into 5 groups exposed to different ultrasound pressure (0，1.0，2. 0，3. 0 and 4. 0 MPa). After 1.5 h of ultrasound exposure, we detected the expression of reactive oxygen species ( ROS) by using full-au­tomatic microplate reader. At 8 h after corresponding interventions, the cell viability, P-selectin and VEGF expression was determined by MTT, immunofluorescence and Western blotting, respectively. Additionally, ROS inhibitor (GSH) or P-se­lectin inhibitor (rPSLG-Ig) were added into the 2. 0 MPa group, and VEGF expression was determined by Western blot­ting, respectively. Results The cell viability presented to be no difference in the 1.0 MPa and 2. 0 MPa groups as com­pared with 0 MPa group (all P >0. 05) , while it decreased significantly in the 3. 0 MPa and 4. 0 MPa groups ( all P < 0.05). The expression of ROS, P-selectin and VEGF increased in the 1.0, 2.0, 3.0, and 4. 0 MPa groups as compared with that of the 0 MPa group (all P <0.05). No difference was found in the expression of ROS, P-selectin and VEGF be­tween the 4. 0 MPa and 3. 0 MPa groups (all P >0. 05) . When GSH or rPSLG-Ig were added in the 2. 0 MPa group , the expression of VEGF was inhibited significantly as compared with that of 2. 0 MPa applied only ( all P < 0. 05 ) . Conclusion Ultrasound-targeted microbubble destruction can increase the expression of VEGF through inducing inflammatory reaction and promote angiogenesis, and 2. 0 MPa is the optimal ultrasound pressure. [ABSTRACT FROM AUTHOR]

Objective To observe the improvement effect of Sanzi Zhike capsule on the lung function in patients with stable COPD, and to explore the possible mechanism of the action. Methods Sixty-eight patients with COPD in stable stage were randomly divided into 2 groups:observation group (treated with Sanzi Zhike capsule,2 capsules each time, three times per day for 6 months, n =33)and control group (treated with placebo, the same dosage, n =35).The lung function detector was used to detect first second forced expiratory volume (FEV1)and forced vital capacity (FVC),forced expiratory volume in 1 second /expected value % (FEV1% pred),and the levels of serum adiponectin (APN),interleu-kin 17 (IL-17),matrix metalloproteinase 9 (MMP-9)and matrix metalloproteinase inhibitor 1 (TIMP-1)were detected before treatment and 6 months after treatment. Results No significant difference was found in FVC, FEV1, FEV1% pred, serum APN, IL-17, MMP-9 and TIMP-1 in the control group as compared with that before treatment (all P >0.05).How-ever, the above indexes all improved in the observation group (all P <0.05)and there were statistically significant differ-ences between the two groups 6 months after treatment (all P <0.05).Conclusion The Sanzi Zhike capsule can improve the lung function in patients with stable COPD, and the mechanism may be that Sanzi Zhike capsule can decrease the levels of the serum APN, IL-17, MMP-9 and TIMP-1. [ABSTRACT FROM AUTHOR]