Visfatin通过线粒体途径抑制胰岛β细胞凋亡

Pancreatic β cell apoptosis inhibited by visfatin via mitochondrial pathways

目的探讨内脏脂肪素（visfatin）对棕榈酸诱导胰岛β细胞凋亡的影响。方法小鼠胰岛β细胞株MIN6体外传代培养，进入对数生长期后进行实验。MTT法检测不同浓度visfatin（0～10^-7mol／L）作用24—72h后MIN6细胞活力变化。流式细胞术检测0．5mmol／L棕榈酸和（或）10^-8mol／Lvisfatin处理24h后MIN6细胞凋亡率的变化；Western blotting检测MIN6抗凋亡蛋白bcl-2、bax、激活型easpase-3和胞质细胞色素C表达的变化。结果Visfatin作用24～48h，MIN6细胞活力呈剂量依赖性增加（P〈0．05）。流式细胞仪检测发现，10^-8mol／Lvisfatin处理24h可明显降低棕榈酸诱导的细胞凋亡率（P〈0．05）；Western blotting结果表明，10^-8mol／Lvisfatin可显著抑制棕榈酸引起的细胞内源性bcl-2表达的下调及激活型caspase-3和胞质细胞色素C表达的上调（P〈0．05）。结论Visfatin可促进胰岛β细胞增殖，并通过细胞内线粒体途径抑制由棕榈酸诱导的胰岛β细胞凋亡。

Objective To investigate the effects of visfatin on palmitate-induced islet β cell apoptosis. Methods Mouse pancreatic cell line MIN6 was performed in vitro serial subcuhivation, and subjected to experiment during exponential phase of growth. Cell viability of MIN6 was detected by MTT assay 24 to 72 h after induction by visfatin with different concentrations （0 to 10^-7 tool/L）. Cell apoptosis rate of MIN6 was examined by flow cytometry after induction by 0.5 mmol/L palmitate and/or 10^-8 mol/L visfatin for 24 h, and expression of bel-2, bax, cleaved caspase-3 and cytochrome C in endochylema was determined by Western blotting. Results Cell viability of MIN6 increased in a dose-dependent manner after treatment with visfatin for 24 to 48 h （P 〈 0.05）. It was revealed by flow cytometry that palmitate-induced apoptosis significantly reduced by 10^-8 mol/L visfatin （P 〈 0.05）. It was demonstrated by Western blotting that 10^-8 mol/L visfatin significantly inhibited the decreased expression of bcl-2 and increased expression of cleaved caspase-3 and cytochrome C induced by palmitate （P 〈 0. 05）. Conclusion Visfatin may promote proliferation of pancreatic β cells, and inhibit palmitate-induced islet β cell apoptosis via mitochondrial pathways.