Advanced glycation end-products (AGEs) are implicated in the pathogenesis of diabetic complications including cardiac dysfunction and heart failure. We aimed to investigate the effects of circulatory AGEs on the oxidative stress parameters in the rat hearts, and also to examine the protective role of gallic acid (GA) in attenuating the AGEs-induced oxidative stress. The experimental Wistar rats were infused with in vitro synthesized rat serum albuminderived AGEs intravenously at a dose of 50mg/kg/day, for 30 days with or without GA. The control animals received equal amount of unmodified rat serum albumin (RSA) intravenously for 30 days. The rats treated with AGEs alone exhibited increased plasma levels of creatine kinase (CK) (p<0.01), and lactate dehydrogenese (LDH) (p<0.001), when compared with controls. In parallel, a significant increase in the levels of the oxidative stress makers lipid peroxides (LPO) (p<0.001), and protein carbonyls (PCO) (p<0.01) were found in AGEs-RSA infused rat hearts compared with control rat hearts. The antioxidant enzymes analysis revealed a significant decrease (p<0.01, respectively) in the activities of superoxide dismutase (SOD) and catalase (CAT) in AGEs-RSA infused rat hearts compared with control rat hearts. Gallic acid co-treatments (administered oral gavage daily at a dose of 25 mg/kg) normalized the decreased levels of antioxidant enzymes in the cardiac tissue on AGEs infusion. The results of the present study provide in vivo evidence that the circulating AGEs induce oxidative stress in the heart, and GA attenuates AGEs-mediated cardiotoxicity.
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