3′,4′-dihydroxyflavonol antioxidant attenuates diastolic dysfunction and cardiac remodeling in streptozotocin-induced diabetic m(ren2)27 rats3u2032,4u2032-dihydroxyflavonol抗氧化变弱舒张功能不全和心脏重塑在体外糖尿病m(高人)27老鼠.pdf

39,4 9-Dihydroxyflavonol Antioxidant Attenuates Diastolic Dysfunction and Cardiac Remodeling in Streptozotocin- Induced Diabetic m(Ren2)27 Rats 1 1 1 1 1,4 3 Fay Lin Khong , Yuan Zhang , Amanda J. Edgley , Weier Qi , Kim A. Connelly , Owen L. Woodman , Henry Krum5, Darren J. Kelly1,2* 1 Department of Medicine, The University of Melbourne, St Vincent’s Hospital Fitzroy, Melbourne, Victoria, Australia, 2 St Vincent’s Institute of Medical Research, St Vincent’s Hospital Fitzroy, Melbourne, Victoria, Australia, 3 School of Medical Sciences, Royal Melbourne Institute of Technology (RMIT) University Bundoora, Melbourne, Victoria, Australia, 4 Department of Medicine, St Michael’s Hospital, Toronto, Ontario, Canada, 5 Department of Epidemiology and Preventive Medicine and Department of Medicine, Faculty of Medicine, Nursing and Health Sciences, Centre of Cardiovascular Research Education (CCRE) in Therapeutics, Monash University, The Alfred, Melbourne, Victoria, Australia Abstract Background: Diabetic cardiomyopathy (DCM) is an increasingly recognized cause of chronic heart failure amongst diabetic patients. Both increased reactive oxygen species (ROS) generation and impaired ROS scavenging have been implicated in the pathogenesis of hyperglycemia-induced left ventricular dysfunction, cardiac fibrosis, apoptosis and hypertrophy. We hypothesized that 39,4 9-dihydroxyflavonol (DiOHF), a small highly lipid soluble synthetic flavonol, may prevent DCM by scavenging ROS, thus preventing ROS-induced cardiac damage. Methodology/Principal Findings: Six week old homozygous Ren-2 rats were randomized to receive either streptozotocin or citrate buffer, then