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目的探讨糖尿病肾脏疾病足细胞是否存在线粒体功能障碍。方法分别从2型糖尿病db/db小鼠及其同窝对照db/m小鼠肾脏中分离足细胞,提取线粒体检测线粒体复合物Ⅰ和Ⅲ功能,提取RNA行实时定量PCR检测足细胞线粒体代谢相关基因的表达;采用免疫组织化学检查检测足细胞标记蛋白WT1的表达。结果 db/db小鼠足细胞线粒体复合物Ⅰ和复合物Ⅲ的活性、线粒体DNA拷贝数均较db/m小鼠低(P均<0.05),db/db小鼠足细胞与线粒体代谢相关的基因SIRT1、PGC-1α、TFAM、NRF1、NRF2以及足细胞标记蛋白nephrin mRNA的表达均较db/m小鼠低(P均<0.05),db/db小鼠足细胞数量较db/m小鼠少(P<0.05)。结论糖尿病小鼠足细胞存在线粒体功能障碍。
Objective To investigate the existence of mitochondrial dysfunction in diabetic foot kidney cells. Methods The podocytes were isolated from the db / db mice of type 2 diabetes mellitus and their littermate db / m mice respectively. Mitochondria were collected to detect the function of mitochondrial complexes Ⅰ and Ⅲ. RNA was extracted and quantitative real - time PCR was used to detect the mitochondrial metabolism of podocytes The expression of podocyte marker protein WT1 was detected by immunohistochemistry. Results The db / db mouse mitochondrial complex Ⅰ and complex Ⅲ activity and mitochondrial DNA copy number were lower than those of db / m mice (all P <0.05). The db / db mouse podocytes were associated with mitochondrial metabolism The expression of genes SIRT1, PGC-1α, TFAM, NRF1, NRF2 and podocyte marker protein nephrin were lower than those in db / m mice (all P <0.05) Less (P <0.05). Conclusion There is mitochondrial dysfunction in podocytes of diabetic mice.