| Summary: | We investigated the effect of cyanidin-3-rutinoside (C3R) against methylglyoxal (MG)-advanced glycation end products (AGEs) mediated cardio-vascular abnormalities in rats pre-treated with MG. In the rats, plasma MG level rose following oral administration of MG (60–120 mg/rat/day) for 8 weeks and was accompanied by a buildup of MG-derived AGE, Nɛ-(carboxymethyl) lysine, in aortic tissue both of which were decreased by co-treatment with C3R (30 and 100 mg/kg/day). Similarly, MG-impaired vascular contraction/relaxation responses were normalized by C3R with concomitant upregulation of endothelial nitric oxide synthase mRNA expression. In the whole animal subjected to coronary artery ligation, C3R (100 mg/kg/day) reduced ventricular extra beats and ventricular tachycardia precipitated during acute ischemic episode. We suggest that C3R reduces the formation and accumulation of AGEs via direct trapping of the MG and upregulation of mRNA expression of glyoxalase I. The findings implicate C3R as a candidate compound for preventing MG-AGE mediated cardiovascular abnormalities in diabetes.
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