.... * P < 0.05, compared with Control.** P < 0.05, compared with GA. Fig. 2. The role of ROS generation and p66shc upregulation in GA-induced inhibition of A375 cell proliferation. (A, B C and D) A375 cells were incubated with 1-10 μg/ml GA for 24 h. Control cells were treated with serum-free...

... remain unclear. Previous study demonstrated the central role of mitochondrial ROS (mtROS) in the pathogenesis of cisplatin nephrotoxicity. The purpose of this study was to explore the mechanism of mtROS regulation in cisplatin nephrotoxicity. Methods: p53, MnSOD and p66shc were detected at mRNA...

... has been shown to attenuate ischemia/reperfusion injury by inhibiting oxidative stress. The present study was carried out to investigate whether the pretreatment of SS31 could reduce hypoxia/reoxygenation (H/R)-induced injury by inhibiting p66Shc. Methods: The cultured rat renal proximal tubular cell...

... and its nitration was potentiated; Gl -PS administration suppressed MnSOD nitration and increased MnSOD and glutathione peroxidase (GPx) activities. Moreover, Gl -PS attenuated the redox enzyme p66Shc expression and phosphorylation dose-dependently in diabetic mice skin. Conclusion. Gl -PS rescued...