Abstract
s / Can J Diabetes 36 (2012) S24eS76 S50 the abundance of NOX2 or p22phox in EC. C3G inhibited glyLDLinduced upregulation of NOX activity and the abundance of NOX2 and p22phox in EC. C3G normalized glyLDL-induced inhibition on mETC Complex I and III enzyme activity and the attenuation of the abundances of NADH dehydrogenase I (Complex I) and cytochrome b (Complex III) in EC. Antibodyof receptor of advanced glycation end products prevented glyLDL-induced changes in NOX and mETC enzymes but did not additively enhance the effects of C3G. The findings suggest that C3G may prevent glyLDL-induced oxidative stress through normalization of the activity of NOX or mETC in vascular EC, which potentially attenuate vascular injury in diabetic condition (supported by CDA and CIHR).
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