抗氧化肽SS-31对高糖诱导的小鼠肾小球系膜细胞凋亡的影响

目的观察抗氧化肽SS-31对高糖诱导小鼠肾小球系膜细胞凋亡的影响。方法将体外培养小鼠肾小球系膜细胞分为正常糖组、正常糖+甘露醇组、高糖组及高糖+SS-31组。采用原位末端转移酶标记技术(TUNEL)及流式细胞术检测细胞凋亡;流式细胞术检测细胞ROS水平;Western blot检测caspase-3、cleaved caspase-3、Bax、Bcl-2、p38 MAPK、p-p38 MAPK及细胞色素C的表达。结果与正常糖组相比,高糖组系膜细胞ROS产生和细胞凋亡明显增加,cleavedcaspase-3和p-p38 MAPK表达增高,Bax/Bcl-2比率明显升高以及细胞色素C易位。SS-31干预能够明显抑制高糖诱导的系膜细胞凋亡和ROS产生,下调cleaved caspase-3和p-p38 MAPK的表达,减少Bax/Bcl-2比率和细胞色素C易位。结论 SS-31能够抑制高糖诱导的系膜细胞凋亡可能是通过减少ROS产生,保护线粒体功能,抑制p38MAPK信号通路激活而实现的。

Influence of antioxidant peptide SS-31 on HG-induced mouse mesangial cells apoptosis

Aim To investigate the effect of antioxidant peptide SS-31 on high glucose(HG)-induced apoptosis in mouse mesangial cells(MMCs).Methods Cultured MMCs were divided into normal glucose group(NG),NG plus mannitol group(M),high glucose group(HG) and HG plus SS-31 group(HG + SS31).Apoptosis of MMCs was analyzed by Dead End Fluorometric TUNEL System and flow cytometry.ROS production was observed by flow cytometry.The expression levels of caspase-3,cleaved caspase-3,Bax,Bcl-2,p38 MAPK,p-p38 MAPK and cytochrome c protein were observed by Western blot.Results Compared with normal glucose group(NG),the production of ROS,the number of cell apoptosis,the expression of cleaved caspase-3 and p-p38 MAPK,ratio of Bax / Bcl-2 and the release of cytochrome c from mitochondria to cytoplasm significantly increased in MMCs in high glucose group(HG).Treatment with SS-31 inhibited HG-induced ROS production,cell apoptosis,expression of cleaved caspase-3 and p-p38 MAPK,ratio of Bax / Bcl-2 and release of cytochrome c from mitochondria to cytoplasm in MMCs.Conclusions SS-31 can prevent HG-induced MMC apoptosis through decreasing ROS production,preserving mitochondrial function and inhibiting activation of p38 MAPK.