Mitochondrial oxidative damage and apoptosis induced by high glucose through Rho kinase signal pathway in renal tubular epithelial cells
- Author:
Wen-Ning LI
1
;
Hui HAN
1
;
Zi-Yang JING
1
;
Xiao-Hong YANG
1
;
Yin ZHANG
1
;
Jia-Li WEI
1
Author Information
- Publication Type:Journal Article
- Keywords: Diabetic nephropathy; Mitochondrial oxidative stress; Rho kinase signal pathway; Tubular epithelial cell
- From: Asian Pacific Journal of Tropical Medicine 2018;11(6):399-404
- CountryChina
- Language:Chinese
- Abstract: Objective: To investigate the role of oxidative stress in human renal tubular epithelial cells (HK-2) induced by high glucose and the underlying signal pathway in vitro. Methods: MYPT1, pro-caspase-3, PGC-1α, and Drp1 protein expressions were measured by Western blot. MnSOD2, Drp1 and PGC-1α mRNA expressions were detected by real time PCR. Results: Results showed that high glucose significantly up-regulated the protein expressions of MYPT1, pro-caspase-3 and the mRNA expression of MnSOD2 in HK-2 cells; while Rho kinase inhibitor fasudil and ROCK1 siRNA inhibited protein expressions of pro-caspase-3 and the mRNA expression of MnSOD2 in HK-2 cells induced by high glucose. Importantly, fasudil and ROCK1 siRNA markedly inhibited the expressions of mitochondrial motor proteins Drp1 and mitochondrial gene PGC-1α in HK-2 cells induced by high glucose. Conclusions: Our findings suggest that Rho kinase signal pathway is involved in mitochondrial oxidative damage and apoptosis in high glucose-induced renal tubular epithelial cells by regulating mitochondrial motor proteins Drp1 and mitochondrial gene PGC-1α. Targeting Rho kinase signal pathway might be a potential strategy for the treatment of diabetic nephropathy. http://www.apjtm.org/article.asp?issn=1995-7645;year=2018;volume=11;issue=6;spage=399;epage=404;aulast=Li;type=2.
