Abstract
In this study we investigated the effect of the xanthine oxidase inhibitor allopurinol on cardiac dysfunction, oxidative‐nitrosative stress, apoptosis, poly(ADP‐ribose) polymerase (PARP) activity, and fibrosis associated with diabetic cardiomyopathy in mice. Diabetes was characterized by increased myocardial, liver and serum XO activity, increased myocardial ROS generation, p22phox, p40phox, p47phox, p91phox mRNA expression, iNOS expression, NT generation, caspase 3/7 and PARP activity/expression, chromatin fragmentation and fibrosis, and declined systolic and diastolic myocardial performance. Allopurinol attenuated the diabetes‐induced increased myocardial, liver and serum XO activities, myocardial ROS, NT generation, iNOS expression, apoptosis, PARP activity and fibrosis, which were accompanied by improved systolic and diastolic performance of the hearts of treated diabetic animals. Thus, XO inhibition with allopurinol improves type I diabetes‐induced cardiac dysfunction by decreasing oxidative/nitrosative stress and fibrosis, which may have important clinical implications for the treatment and prevention of diabetic cardiomyopathy and vascular dysfunction.
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