作者: Renu A. Kowluru , Vibhuti Kowluru
DOI:
关键词:
摘要: PURPOSE: Increased superoxide levels are implicated in the pathogenesis of diabetic retinopathy. We have shown that functional activation a small molecular weight G-protein, H-Ras, is one signaling steps involved glucose-induced apoptosis retinal capillary cells. The goal this study was to elucidate mechanism(s) by which oxidative stress could result H-Ras diabetes. METHODS: Experiments were performed isolated endothelial cells treated with H(2)O(2), or accumulation inhibited either dismutase mimetic (MnTBAP) overexpressing mitochondrial (MnSOD). vitro experiments complemented vivo using retina from mice MnSOD. RESULTS: H(2)O(2) activated and its downstream pathway, including Raf-1 phosphorylation p38 (p-p38) MAP kinase. Inhibition significantly attenuated p-p38 Overexpression MnSOD prevented diabetes-induced both CONCLUSIONS: Our results clearly indicate pathway vasculature be under control superoxide, diabetes can inhibiting accumulation.