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To examine the regulatory mechanisms of oligopeptides derived from soft-shelled turtle protein on tubulin activity in tumor cells, this study employed three specific oligopeptides D-7-A, E-7-W, and G-8-V obtained from soft-shelled turtle protein. The objective was to assess their impact on tubulin polymerization and depolymerization, investigate their interaction with tubulin, and elucidate the mechanisms induce apoptosis in tumor cells. The results showed that the three oligopeptides exhibited similarities to vincristine and acted as inhibitors of tubulin polymerization, their respective IC50 values was 3.72, 5.01, and 5.95 µmol/L. Furthermore, the molecular docking analysis revealed that D-7-A interacted with the active center of α-tubulin 4X1I, specifically binding to Ser178 and Thr179. The active center of E-7-W was found to be bound by Gln15, Thr225, Tyr224, Tyr210 and Arg214. Similarly, G-8-V was observed to bind to Gln11, Ser178 and Asp329 at the active center, exerting a significant impact on α-tubulin. The results of cell experiments showed that D-7-A, E-7-W and G-8-V had dose-dependent inhibitory effects on A549 cells, with IC50 values of 2003±72, 1877±102 and 1789±137 μmol/L, respectively. The G-8-V exhibited the most potent inhibitory effect on A549 cells, leading to the induction of apoptosis. Moreover, the apoptosis rate demonstrated a significant increase with prolonged drug treatment time. The underlying mechanism of action involved the inhibition of tubulin polymerization and the induction of apoptosis by perturbing the valence bond of α-tubulin. [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.)

Objective To explore the protective effect of miR‐499 on myocardial ischemia‐reperfusion injury and its possible mechanism from the aspect of mitochondrial autophagy. Methods Myocardial cell H9c2（2‐1） was induced by ischemia/reperfusion （I/R）, and hypoxia/reoxygenation （H/R） myocardial cell model was established. The cells were treated with miR‐499 mimics and/or P110. The cells were divided into BC group, I/R group, I/R + mi group, I/R + NC group, I/R + mi + P110 group and I/R + NC + P110 group. Cell proliferation was detected by CCK8 method. ROS, mitochondrial membrane potential and apoptosis were detected by flow cytometry. MDA, SOD and ATP contents were detected by their kit. The mRNA and protein expression levels of mitochondrial fusion, division and autophagy related genes Fis1, Mfn1, Parkin, LC3‐Ⅱ, p62 and Drp1 were detected by qRT‐PCR and Western blot. Mitochondrial autophagy was observed by transmission electron microscope. Results miR‐499 mimics and/or P110 can reduce the proliferation inhibition rate and apoptosis rate of myocardial cells induced by I/R. The mitochondrial membrane potential decreased. The mitochondrial autophagy decreased and the ATP content increased. The gene and protein expression levels of Fis1, Parkin, LC3‐Ⅱ and Drp1 decreased, while those of Mfn1 and p62 increased. The content of ROS and MDA in cells decreased, but the content of SOD increased. Conclusions miR‐ 499 can reduce the occurrence of oxidative stress by reducing mitochondrial autophagy mediated by Drp1, thus protecting I/R‐induced cardiomyocytes. [ABSTRACT FROM AUTHOR]

BACKGROUND: Rehmannia glutinosa has the effects of inhibiting oxidative stress, inhibiting apoptosis, inhibiting nerve inflammation, promoting angiogenesis and anti-aging, and has unique advantages in the treatment of ischemic stroke. The combination of Rehmannia glutinosa with mesenchymal stem cells as a carrier can play a better role in the treatment of ischemic stroke. OBJECTIVE: To review the research progress of Rehmannia glutinosa combined with mesenchymal stem cells in the treatment of ischemic stroke. METHODS: We searched CNKI and PubMed for the literature on the treatment of senile ischemic stroke with Rehmannia glutinosa combined with mesenchymal stem cells from 2012 to 2022. The keywords were “Rehmannia, mesenchymal stem cells (MSCs), ischemic stroke” in Chinese and English, respectively. Finally, 86 articles were included for further review. RESULTS AND CONCLUSION: (1) The mechanisms of mesenchymal stem cells in the treatment of ischemic stroke were reviewed, including the promotion of cell migration and differentiation, immunomodulation, and inhibition of apoptosis. (2) The mechanisms of Rehmannia glutinosa in treating ischemic stroke were summarized, including inhibition of oxidative stress, inhibition of nerve inflammation, inhibition of apoptosis, promotion of neuroangiogenesis, and anti-aging. (3) Rehmannia glutinosa could stimulate the vitality of mesenchymal stem cells, promote the proliferation of mesenchymal stem cells, induce the differentiation of mesenchymal stem cells into neuron-like cells, and improve the survival rate of mesenchymal stem cells in vivo, so as to achieve the goal of synergistic treatment of ischemic stroke. (4) The mechanism of Rehmannia glutinosa combined with mesenchymal stem cells in the treatment of ischemic stroke was summarized, including inhibition of oxidative stress, inhibition of apoptosis, anti-aging, promotion of angiogenesis and nerve remodeling, thereby providing theoretical reference for the new treatment of ischemic stroke in the future. [ABSTRACT FROM AUTHOR]

To investigate the effects of matrine on P2X3 receptor, pain behavior and pain threshold in neuropathic rat dorsal root ganglion. Thirty Sprague-Dawley male rats were randomly divided into 3 groups, including model group, experimental group and sham operation group. One day after successful modeling, the experimental group was given 30 mg/ (kgod) intraperitoneal injection of matrine solution, once a day; Sham operation group and model group were given intraperitoneal injection of 0.9% sodium chloride solution once a day for 14 days. Spontaneous pain behavioral score, mechanical pain threshold, thermal pain threshold, P2X2 and P2X3mRNA relative expression levels, P2X2 and P2X3 protein expression levels, and oxidative stress index levels were detected. The scores of spontaneous pain behavior in both the model group and the experimental group were higher than those in the sham operation group. Since the 5th day after surgery, the scores of spontaneous pain behavior in the experimental group were lower than those in the model group(P<0.05). Compared with the sham operation group, the mechanical pain threshold and thermal pain threshold in the model group were decreased from the 3rd day after surgery, while the mechanical pain threshold and thermal pain threshold in the experimental group were increased from the 5th day after surgery (all P<0.05). There were no differences in mechanical pain threshold and thermal pain threshold between experimental group and sham operation group on day 14 after surgery (P>0.05). P2X2 and P2X3 mrna, P2X2 and P2X3 proteins in model group were higher than those in sham operation group and experimental group (P<0.05), but there were no differences in P2X2, P2x3 mRNA, P2X2 and P2x3 proteins between experimental group and sham operation group (P>0.05). SOD and MDA of spinal cord in model group were lower and higher than those in sham group before intervention and 1 and 2 weeks after intervention. SOD and MDA of spinal cord tissue of experimental group were higher than those of model group (all P<0.05). Matrine can effectively relieve mechanical and thermal pain induced by neuropathic pain, and has good analgesic effect. The mechanism may be that matrine can reduce P2X2 and P2X3 receptors in dorsal root neurons of rats, and it also plays a role in inhibiting oxidative stress response of spinal cord tissue of neuropathic rats. It is closely related to the inhibition of neuronal apoptosis in spinal cord of neuropathic pain rats. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of circ_0016788 targeting miR-338-3p on the proliferation, apoptosis, migration and invasion of prostate cancer cells. Methods circ_0016788 and miR-338-3p expressions were detected by RT-qPCR in prostate cancer tissues.si-circ_0016788, si-NC, miR-NC, miR-338-3p mimic, si-circ_0016788+anti-miR-NC, si-circ_0016788+ anti-miR-338-3p were transfected into DU145 cells respectively. CCK-8, Transwell method and flow cytometry were applied to detect DU145 cells growth, migration, invasion and apoptosis rate. The interaction between circ_0016788 and miR-338-3p was confirmed by dual luciferase reporter assay. Results circ_0016788 was highly expressed（P＜0.05） while miR-338-3p was lowly expressed（P＜0.05） in prostate cancer tissues. After inhibiting the expression of circ_0016788, the cell inhibition rate, apoptosis rate and miR-338-3p expression level were increased（P＜0.05）, and the numbers of migration and invasion were decreased（P＜0.05）. After overexpression of circ_0016788, the cell inhibition rate and apoptosis rate were decreased（P＜0.05）, and the numbers of migration and invasion were increased（P＜0.05）. miR-338-3p was a direct target gene of circ_0016788. Inhibition of miR-338-3p expression significantly attenuated the effects of circ_0016788 low expression on DU145 cells inhibition rate, migration and invasion number, and cell apoptosis rate（P＜0.05）. Conclusion Inhibition of circ_0016788 can induce prostate cancer cell apoptosis and inhibit proliferation, migration and invasion by promoting miR-338-3pexpression. [ABSTRACT FROM AUTHOR]

BACKGROUND: Fibronectin type III domain containing 5 (FNDC5) is a protein molecule that regulates glycolipid metabolism, regulates cell apoptosis and participates in the inhibition of atherosclerosis. OBJECTIVE: By constructing a lentiviral vector overexpressing FNDC5 for transfecting human umbilical vein endothelial cells, to verify the effect of FNDC5 in regulating endothelial cell apoptosis. METHODS: The lentiviral vector overexpressing FNDC5 was constructed. Human umbilical vein endothelial cells in logarithmic growth phase were cultured and divided into three groups: blank group was not transfected with lentivirus, control group was transfected with an empty vector lentivirus without FNDC5, and experimental group was transfected with the lentiviral vector overexpressing FNDC5. At 7 days after transfection, RT-PCR and western blot were used to detect the mRNA and protein expression of FNDC5. After 7 days of transfection, oxidized low-density lipoprotein solution was added to the three groups of cells, and the cell viability was determined by cell counting kit-8 method, and cell apoptosis was detected by Hoechst 33342/PI double staining and flow cytometry. RESULTS AND CONCLUSION: The mRNA and protein expressions of FNDC5 in the experimental group were higher than those in the blank and control groups (P < 0.05). Cell counting kit-8 test results showed that the cell viability in the experimental group was higher than that in the blank and control group at 1 and 2 hours after addition of oxidized low-density lipoprotein (P < 0.05). However, there was no significant difference in the cell viability between the three groups at 4 hours after addition of oxidized low-density lipoprotein (P > 0.05). Flow cytometric results showed that the apoptotic rate was lower in the experimental group than the blank and control group at 24 hours after addition of oxidized low-density lipoprotein (P < 0.05). Hoechst 33342/PI double staining results showed that the number of apoptotic cells in experimental group was less than that in the blank and control groups. To conclude, overexpression of FNDC5 could inhibit the apoptosis of human umbilical vein endothelial cells. [ABSTRACT FROM AUTHOR]

BACKGROUND: Stem cells, especially extracellular vesicles derived from mesenchymal stem cells, have the potential to promote regeneration in different renal injury models. OBJECTIVE: To review the application progress of extracellular vesicles derived from mesenchymal stem cells in preclinical models of acute and chronic renal injuries and the latest data in renal transplantation. In addition, new engineering strategies to improve the therapeutic effect of extracellular vesicles were discussed. METHODS: CNKI, Wanfang, and PubMed databases were searched. The Chinese search words included “acute renal injury, chronic kidney disease, extracellular vesicles, exosomes”. English search words included “acute renal injury, chronic kidney disease, extracellular vesicles, exosomes, regeneration”. The search literature was the original research works and reviews. The retrieval time limit was from the establishment of the database to 2021, and 82 articles were selected for analysis and summary. RESULTS AND CONCLUSION: (1) The research on mesenchymal stem cell derived extracellular vesicles in the treatment of renal injury has been widely carried out. Animal experiments have confirmed that mesenchymal stem cell derived extracellular vesicles can play a renal protective role and delay the progress of disease in the treatment of acute and chronic renal injuries. The specific mechanism involves the reprogramming of injured cells, cell proliferation, angiogenesis and inhibition of apoptosis and inflammation. Immediate administration of extracellular vesicles after renal transplantation can improve acute and chronic ischemia-reperfusion injuries. (2) There are few clinical trials on the treatment of nephropathy with mesenchymal stem cell-derived extracellular vesicles. One clinical trial observed that one year after taking umbilical cord blood mesenchymal stem cell-derived extracellular vesicles, the renal function of patients with chronic kidney disease was improved. (3) Based on the above research, mesenchymal stem cells derived extracellular vesicles will help to provide a new experimental model and basis for the effective treatment and repair of acute and chronic renal injuries, and open up a new direction for the clinical treatment of renal diseases. [ABSTRACT FROM AUTHOR]

Renal cell carcinoma is one of the most common malignancies in genitourinary cancers. In China, the incidence of renal cell carcinoma has been increasing year by year. Regulated cell death is a cell-independent and orderly death controlled by genes, which is ubiquitous in organisms and plays a crucial role in maintaining the cell homeostasis. Recently, cuproptosis was reported in Science, which further reinforced the importance of cell death in living organisms. With the increasing understanding of regulated cell death, more and more studies have shown that regulated cell death (such as ferroptosis, autophagy, pyroptosis) is closely related to the tumorigenesis and development of renal cell carcinoma. For example, induction of ferroptosis inhibits the invasion and metastasis of renal cell carcinoma and is closely related with better prognosis; pyroptosis not only induce renal cancer cell death and also activate the immune-response against renal cancer; autophagy plays a "bidirectional" role in renal cell carcinoma, which can inhibit the growth of renal cell carcinoma cells but may weaken the efficacy of combinational therapy; inhibition of apoptosis and necrotizing apoptosis can significantly promote the proliferation and invasion of renal cell carcinoma. This review has summarized the molecular mechanisms of ferroptosis, pyroptosis, autophagy, apoptosis and necrotizing apoptosis and the advances of different regulatory cell death in the tumorigenesis and development of renal cell carcinoma to provide a new perspective for exploring the mechanisms of tumorigenesis and potential targets of treatment. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect and mechanism of ursodeoxycholic acid (UDCA) on the injury of H9c2 cardiomyocytes induced by doxorubicin (DOX). Methods: H9c2 cells were cultured in vitro, H9c2 was treated with 1μM DOX and different concentrations of UDCA, cell viability was determined by CCK-8 method; real-time quantitative polymerase chain reaction was used to detect the expression of cardiomyocyte apoptosis molecule Bax and inflammatory factors IL-1β and IL-6; Western blotting was used to detect the changes in the expression levels of UDCA on DOX-induced cardiomyocyte apoptosis-related proteins Bax, Bcl2, and Caspase3. Results: Compared with the control group, the cardiomyocyte viability of the DOX group was weakened; the expression of inflammatory factors IL-1β and IL-6 were up-regulated; the expression of pro-apoptotic molecules Bax and cleaved Caspase3 were increased; the apoptosis-inhibiting protein Bcl2 was down-regulated (P<0.05). Compared with the DOX group, the UDCA+DOX group significantly restored the vitality of cardiomyocytes; the expression of inflammatory factors IL-1β and IL-6 was down-regulated; the pro-apoptotic molecules Bax and cleaved Caspase3 were down-regulated; the expression of inhibiting apoptosis protein Bcl2 was up-regulated (P<0.05) . Conclusion: UDCA can alleviate the damage of H9c2 cardiomyocytes induced by DOX, and its mechanism may be related to the inhibition of inflammation and apoptosis. This study provides a new experimental basis and theoretical basis for the prevention and treatment of doxorubicin myocardial toxicity. [ABSTRACT FROM AUTHOR]

BACKGROUND: Studies have shown that treatment with triptolide reduces ischemic lesion area, water content, and nerve cell death in a rat model of stroke. In addition, triptolide can promote the repair of spinal cord injury by inhibiting astrocyte hyperplasia, microglia activation and inflammatory response. OBJECTIVE: To investigate the effect of triptolide on the autophagy and apoptosis in the spinal cord of Thy-YFP transgenic mice after spinal cord injury. METHODS: Sixty Thy-YFP transgenic mice were randomly divided into four groups: sham, dimethyl sulfoxide (DMSO), triptolide and methylprednisolone groups. Following the establishment of the spinal cord injury models, mice in the triptolide, DMSO and sham group were immediately intraperitoneally injected with triptolide (0.2 mg/kg·d) or 5% DMSO-normal saline solution (0.2 mg/kg·d) for 7 days, whereas mice in the methylprednisolone group were intraperitoneally injected with methylprednisolone (30 mg/kg) at 30 minutes, 6 hours and 24 hours after surgery. Basso Mouse Scale was used to assess the recovery of motor function; hematoxylin-eosin staining and Nissl staining were used to explore tissue recovery after spinal cord injury; western blot and immunofluorescence staining were employed to assess the levels of autophagy-associated proteins, Beclin-1, LC3B, p62, and apoptosis-associated proteins, Bcl-2, Bax and caspase-3. An ethic approval for animal experiments was obtained from Hebei North University with an approval No. W20200002. RESULTS AND CONCLUSION: Treatments with triptolide or methylprednisolone after spinal cord injury significantly improved motor function and reduced neuronal cell death. In addition, the expression of autophagy-associated protein LC3B was upregulated and the expression of p62 was downregulated following triptolide treatment; the expressions of apoptosis-associated proteins caspase-3 and Bax were reduced, while the expression of anti-apoptosis protein Bcl-2 was increased after triptolide treatment. To conclude, triptolide improves the motor function after spinal cord injury, which is related to upregulation of autophagy and inhibition of apoptosis. Triptolide may be a potential neuroprotective agent for spinal cord injury. [ABSTRACT FROM AUTHOR]

BACKGROUND: Previous studies have shown that various miRNAs play a role in bone formation. miR-335-5p can protect osteoblasts from oxidative stress and protect osteoblasts under induction with ferric ammonium citrate, but the effect of miR-335-5p on osteoblast proliferation and apoptosis in high glucose environments is unknown. OBJECTIVE: To investigate the effect of miR-455-3p targeting HIPK2 on proliferation and apoptosis of osteoblasts induced by high glucose. METHODS: Dualluciferase reporter assay was used to verify the targeting of miR-455-3p to HIPK2. MC3T3-E1 cells were induced by high glucose in vftro, and MC3T3-E1 cells were treated as follows: blank group, high glucose group, high glucose+miR-control group, high glucose+miR-455-3p group, high sugar+si-control group, high sugar+si-HIPK2 group, high glucose+miR-455-3p+pcDNA group and high glucose+miR-455-3p+pcDNA-HIPK2 group. The expression of miR-455-3p and HIPK2 mRNA was detactad by qRT-PCR, cell viability was detected by MIT assay, apoptosis was detected by ftow cytometry, and the expression of HIPK2, p-STAT3 and STAT3 protein was detected by western blot. RESULTS AND CONCLUSION: HIPK2 was a target gene of miR-455-3p, and miR-455-3p negatively regulated the expression of HIPK2. High glucose treatment inhibited the expression of miR-455-3p and promoted the expression of HIPK2. The over-expression of miR-455-3p or the inhibition of HIPK2 promoted MC3T3-E1 survival and inhibit cell apoptosis after high glucose treatment. The over-expression of HIPK2 partially reversed the survival promotion and apoptosis inhibition of miR-455-3p on osteoblasts induced by high glucose. miR-455-3p inhibited the expression of p-STAT3 in osteoblasts by regulating HIPK2. To conclude, miR-455-3p inhibits the apoptosis and promotes the proliferation of osteoblasts induced by high glucose via down-regulating HIPK2, which may be related to the inhibijion of STAT3 signaling pathway. [ABSTRACT FROM AUTHOR]

Objective: To investigate the therapeutic effect of recombinant human brain natriuretic peptide on pathological brain injury and cognitive dysfunction in septic mice, and to clarify its mechanism of brain protection. Methods: The cecum ligation puncture method (CLP) septic mice model was established. rhBNP was injected subcutaneously 6 hours after CLP surgery, and the same volume of saline was used as a control for 14 days, once daily. The basic motion state, exploration ability and anxiety of animals were evaluated by open-field experiment. The conditional fear test was used to detect the changes in the contextual memory of animals. TUNEL staining was used to detect the apoptosis of nerve cells in CA1 region of hippocampus. Western blotting was used to detect the expression levels of TNF-α, caspase-8 and caspase-3 in hippocampal tissues. Results: In the open-field test, the mice in the CLP+Veh group had a significant decrease in average movement speed(P<0.0001), the number of line crossing within 5 min(P<0.0001), and the movement time in the central region (P<0.0001) when compared with that in the Sham+Veh group. There were no statistically significant differences in average movement speed (P=0.35) and the number of line crossing within 5 min (P=0.064) after rhBNP treatment in the CLP+rhBNP group, but the movement time in the central region was significantly increased (P=0.0005) when compared with that in the CLP+Veh group. In the condition-related fear test, the percentage of freezing time of mice in the CLP+Veh group was significantly reduced when compared with that in the Sham+Veh group (P<0.0001). The percentage of freezing time of mice in the CLP+rhBNP group was significantly increased when compared with that in mice from CLP+Veh group(P=0.0014). CLP-induced septic mice showed neuronal apoptosis of hippocampal CA1 region. rhBNP therapy can significantly reduce brain pathological changes and reduce neuronal apoptosis by inhibiting the TNF-acaspase- 8 signaling pathway upstream of caspase-3. Conclusions: Therefore, The mechanism of rhBNP treatment for SAE may be related to inhibition of neuronal apoptosis. [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 the effect of RACK1 on Bordzomib(Bor) induced apoptosis and MAPK/ERK pathway in multiple myeloma(MM) cells. Methods: 6 cases of MM patients admitted to the First People’s Hospital of Yueyang and 6 normal subjects were selected. Real-time quantitative PCR was used to detect the expression of RACK1 m RNA in the plasma and human MM cell lines. MM cells were divided into 3 groups: control group(no intervention), Bor group(75 nM Bor intervention for 12 h) and Bor+siRACK1 group(RACK1 si RNA transfection for 24 h followed by Bor intervention). The cell viability of each group were detected by CCK-8 method, the apoptosis was detected by Hoechest 33342 staining, and the expressions of MAPK/ERK pathway-related proteins were detected by Western Blot. Results: Compared with normal subjects, RACK1 m RNA expression was significantly increased in the plasma of MM patients and human MM cell lines(P<0.05). Bor significantly reduced the viability of MM cells at 12 h, 24 h and 48 h(P<0.05). Compared with the control group, the viability in the Bor group and the Bor+siRACK1 group were significantly lower than that of the Bor group(P<0.05). Hoechest 33342 staining showed that the control group had uniform nuclear staining, and no apoptotic bodies was found, while a small number of apoptotic bodies were found in the Bor group, a large number of apoptotic bodies were observed in the Bor+siRACK1 group, which showed nuclear pyknosis or fragmentation. Compared with the control group, the apoptotic rate of MM cells in the Bor group and the Bor+siRACK1 group were significantly increased(P<0.05), and the apoptotic rate of MM cells in the Bor+siRACK1 group was significantly higher than that in the Bor group(P<0.05). Compared with the control group, the expressions of p-P38 and p-ERK were significantly decreased in the Bor group and the Bor+siRACK1 group, and the expression of p-P38 and p-ERK in the Bor+siRACK1 group was lower than the Bor group(P<0.05). There were no significant difference in the expressions of P38 and ERK among the 3 groups(P>0.05). Conclusions: RACK1 silencing enhances Bor-induced apoptosis and growth inhibition of MM cells, and its mechanism may be related to the inhibition of MAPK/ERK pathway. [ABSTRACT FROM AUTHOR]

Objective To observe the effect of puerarin on osteoblasts apoptosis induced by pioglitazone． Methods Cell proliferation activity of MC3T3-E1 cells on different concentrations of puerarin(0. 01 － 100 μmol /L) and pioglitazone(20 μmol /L) after 24 hours was detected by MTT method． Cell apoptosis of MC3T3-E1 cells on puerarin and pioglitazone was detected by flow cytometry． The expression of apoptosis related proteins caspase-3，caspase-8，Bcl-2 and Bax was detected by Western blot． Results 1． Compared with the control group，cell proliferation activity of pioglitazone group was obviously decreased (P ＜ 0. 05)，but that of 0. 1 － 10 μmol /L puerarin group was obviously increased (P ＜ 0. 05)． 2． Compared with the pioglitazone group，cell proliferation activity was obviously increased after 0. 1 － 1 μmol /L puerarin was added (P ＜ 0. 05)． 3． The apoptosis rate increased by pioglitazone was inhibited after 1 μmol /L puerarin was added (P ＜ 0. 05)． 4． Pioglitazone enhanced caspase-3， caspase-8 and Bax protein expression and decreased Bcl -2 protein expression． But caspase-3 protein expression was decreased and Bcl-2 protein expression was increased after puerarin was added． Conclusion Puerarin can inhibit the osteoblasts apoptosis induced by pioglitazone． [ABSTRACT FROM AUTHOR]

Objective To study the clinical significance of serum Survivin and DcR3 levels in patients with cervical cancer. Methods 91 cases of cervical squamous cell carcinoma patients were enrolled in this study, there were 34 cases in stage I, 33 cases in stage II, 24 patients in stage III. The serum levels of CA125, CA19-9, CEA, Survivin and DcR3 were tested. Results The serum levels of CA125, CEA in stage II were significantly higher than the stage I (P<0.05) . The serum levels of CA125, CA19-9, CEA of stage III were significantly higher than stage I, II (P < 0.05) . Survivin, DcR3 of stage II patients than stage I significantly increased (P < 0.05) . The serum levels of Survivin, DcR3 of stage III were significantly higher than stage I, II (P < 0.05) . The serum levels of Survivin and CA125, CEA showed significant positive correlation (P<0.05), and CA19-9 showed no significant correlation (P < 0.05), The serum levels of DcR3 with CA125, CEA showed significant positive correlation (P < 0.05) . Conclusion Survivin and DcR3 disorder is closely associated with cervical cancer staging, combining with conventional tumor markers would help to determine the progress of the disease. [ABSTRACT FROM AUTHOR]

Objective To apply the small interfering RNA (siRNA) targeting survivin to inhibit expression of survivin gene in HSC-3 oral squamous cell carcinoma and to increase the apoptosis of HSC-3 cells. Methods siRNA was synthesized and transfected into oral squamous cell carcinoma HSC-3 cells. Compared with negative control group and blank control group, semi-quantitive reverse transcription-polymerase chain reaction (RT-PCR) was used to detect survivin mRNA. Cellular viability was detected by MiT and HSC-3 cell apoptosis was determined by tunnel and flow cytometry. Results Expression of survivin mRNA was decreased significantly in siRNA group compared with negative control group and blank control group. Cellular viability was not affected in negative control group and blank control group, but cellular viability in siRNA group was significantly decreased. As to the cellular apoptosis rate, the transfected group (24.99%±l.33%) was significantly higher than negative control group (1.24%±0.13%) and blank control group (0. l0%±0.02%). Conclusion Survivin gene silenced by siRNA might promote apoptosis of oral squamous cell carcinoma. Survivin siRNA gene therapy would become a new target point for oral squamous cell carcinoma. [ABSTRACT FROM AUTHOR]