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Objective To investigate the protective effect of FLPNF and the improvement of glucose-stimulated insulin secretion against dexamethasone-induced apoptosis of islet cells. Methods INS-1 cells were treated with oligopeptide FLPNF and dexamethasone, either separately or in combination. Proliferation of INS-1 cells in each group was assessed with CCK-8 assay and the insulin secretion stimulated by glucose was detected by ELISA. The apoptotic condition of the cells was observed and assessed with TUNEL and the apoptosis rate of each group was detected using flow cytometry. The expression of major target protein molecules related to apoptosis and Glut2 was detected by Western blotting analysis. Results Dexamethasone inhibited the growth of INS-1 cells in the group treated with dexamethasone. Cell damage was obvious with observable nuclear shrinkage and nuclear rupture. In addition, apoptosis rate was found to be 40.6％±2.4％. The expression of the apoptosis-related protein Bcl-2 and Glut2 was significantly reduced, whereas that of Bax and caspase-3 was significantly increased. After the combined treatment of oligopeptide FLPNF and dexamethasone, the results were reversed, and the apoptosis rate declined to 27.2％±2.0％ (P ＜ 0.001), cell morphology was improved, and the expression of apoptosis-related protein molecules of islet cells and protein Glut2 was significantly improved. Conclusion FLPNF has the ability of protecting islet cells from dexamethasone-induced apoptosis and improving the glucose-stimulated insulin secretion of islet cells.
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Objective To study the effects of ω-3 fatty acid on liver function in patients undergoing hepatectomy. Methods A PubMed, Embase and Cochrane Library database search was performed to retrieve all of the randomized controlled trial (RCT) evaluating the value of perioperative ω-3 fatty acid in patients undergoing hepatectomy until the end of September 2016. Data extraction and quality assessment of RCT were performed in accordance with PRISMA guidelines. The quality of evidence for each postoperative outcome was assessed using the GRAD Profiler system. A random-effects model was used to conduct a Meta-analysis with RevMan 5.3.5 software. Results Five documents were identified according to the inclusion criteria. Meta- analysis results showed that ω- 3 fatty acid significantly reduced the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) on the third day of the operation in patients undergoing hepatectomy: mean difference ( MD ) = -74.89 and-60.87, 95% CI-110.02?39.76 and-96.05?-25.68, P＜0.01; ω-3 fatty acid significantly increased the level of prealbumin (Pre-Alb) on the third day of the operation: MD＝9.61, 95% CI 4.22?15.00, P＜0.01; but ω-3 fatty acid did not improve the levels of total bilirubin (TBil) and albumin (Alb) on the third day of the operation: MD=-1.13 and 1.16, 95% CI-2.48?0.21 and-0.35?2.68, P＞0.05. Conclusions The ω-3 fatty acid is potentially beneficial in reducing the levels of ALT and AST, and increases the level of Pre-Alb on the third day of the operation in patients undergoing hepatectomy, but does not improve the levels of TBil and Alb.
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Objective To elucidate the inhibitory effect of SGI-1027 on cell proliferation and apoptosis of Huh7 cells.Methods Huh7 cells were treated with different concentrations (0,5,10,15,20,25,30,and 35 μ mol/L) of SGI-1027 for 24 h.MTS assay was performed to detect cell proliferation.Huh7 cells treated with 0.1％ DMSO were used as the control group,and those treated with 30 μmol/L SGI-1027 as the experimental group.Flow cytometry was performed to study the cell cycle,and Annexin V-FITC/PI detection for studying cell apoptosis.TUNEL staining was performed to observe changes in cell morphology.Results The results of the MTS assay revealed that SGI-1027 significantly inhibited the proliferation of Huh7 cells in a dose-dependent manner,and the IC50 was 27.3 μmol/L.SGI-1027 did not block the cell cycle of Huh7 cells,but induced cell apoptosis in Huh7 cells.The rates of apoptosis were 3.242％ ± 0.204％ in the control group and 46.57％ ± 2.512％ in the experimental group (P ＜ 0.05).In the experimental group,typical apoptotic nucleus alterations were observed by fluorescence microscopy after TUNEL staining.The percentage of apoptotic cells was 1.077％ ± 0.407％ in the control group and 58.24％ ± 8.427％ in the experimental group (P ＜ 0.05).Condusion SGI-1027 inhibits Huh7 cell proliferation and induces apoptosis in vitro.
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Objective To investigate the expression characteristics of Golgi phosphoprotein 3(GOLPH3)in human hepatocellular carcinoma (HCC)and explore its clinicopathological significance. Methods The expressions of GOLPH3 protein was detected in 132 cases of paired paraf-fin embedded HCC specimens and pericarcinoma tissues using immunohistochemical staining ,and the relation of the expression of GOLPH3 to clinicopathologic features was analyzed. Meanwhile,the expression and distribution of GOLPH3 in HCC cells was observed by laser confocal mi-croscopy. Results The positive expression rates of GOLPH3 in HCC and pericarcinoma tissues were 70.0%(92/132)and 42.4%(56/132) (P<0.001),respectively. The incidence of portal vein tumor thrombus in high and low GOLPH3 expression groups of HCC were 21.2%(14/66) and 6.1%(4/66)(P<0.05),respectively. The expression rate of GOLPH3 in HCC was significantly higher than that in pericarcinoma tissues, and the expression of GOLPH3 in HCC was positively related to portal vein tumor thrombus. In addition ,GOLPH3 was mainly expressed in cyto-plasm of HCC cells,and there was also scattered distribution in the nucleus. Conclusion GOLPH3 acts as an oncogene and may play vital roles in the carcinogenesis and development of HCC.