肾小管上皮细胞线粒体氧化损伤在肾间质纤维化中的作用及机制.docVIP

肾小管上皮细胞线粒体氧化损伤在肾间质纤维化中的作用及机制 目录 TOC \o 1-9 \h \z \u 目录 1 正文 1 文1：肾小管上皮细胞线粒体氧化损伤在肾间质纤维化中的作用及机制 1 2 结果 4 3 讨论 5 文2：血管紧张素Ⅱ在肾间质纤维化中的作用机制 6 1 AngⅡ与AngⅡ受体（ATR） 7 2 AngⅡ与TGF-β1 8 4 AngⅡ与表皮生长因子受体（ECGR） 10 5 AngⅡ與低氧诱导因子-1α（HIF-1α） 11 6 AngⅡ与MicroRNA（ miRNA） 12 参考文摘引言： 13 原创性声明（模板） 14 文章致谢（模板） 15 正文 肾小管上皮细胞线粒体氧化损伤在肾间质纤维化中的作用及机制 文1：肾小管上皮细胞线粒体氧化损伤在肾间质纤维化中的作用及机制 [Abstract] Objective To discuss the effect and mechanism of mitochondria oxidative damage in renal tubular epithelial cells on renal intetitial fibrosis. Methods A total of 60 health male rats were selected from a local animal experimental center from June to December 2015 and divided into study group and control group. Rats in the study group were given left ureteral obstruction， while those in the control group were only given left ureteral mobilization. Paramete including the expression of genes in mitochondria and renal function of the left kidney were detected and analyzed after 14 days. Results At 14 d after surgery， the expression levels of mtDNA （±）， regenerating gene （±）， interrupted gene（±）， and fusion gene（±， ±） in the study group were all significantly higher than those（±， ±， ±， ±， and ±） in the control group（P）. The level of COX （±） in kidney tissues in the study group was significantly higher than that（±） in the control group， while the level of SOD was significantly lower than the control group（± vs ±）. The RIF index （±） in the study group was significantly higher than that （±） in the control group （P）. Conclusion Mitochondria oxidative damage in renal tubular epithelial cells has a significant effect on renal intetitial fibrosis. Mitochondria oxidative damage caused by anoxia may lead to functional impairment of kidney tubules， inducing a large number of fibrosis facto and resulting in renal intetitial fibrosis from multiple pathways。 [Key words] Renal intetitial fibrosis； Renal tubular epithelial cell； Mitochondria oxidative damage； Renal tubular function 绝大部分慢性肾脏