Mitochondrial oxidative damage and apoptosis induced by high glucose through Rho kinase signal pathway in renal tubular epithelial cells
Asian Pacific Journal of Tropical Medicine
; (12): 399-404, 2018.
Article
in Chinese
| WPRIM (Western Pacific)
| ID: wpr-972452
Responsible library:
WPRO
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.
Full text:
Available
Database:
WPRIM (Western Pacific)
Language:
Chinese
Journal:
Asian Pacific Journal of Tropical Medicine
Year:
2018
Document type:
Article