Betanin ameliorates isoproterenol-induced acute myocardial infarction through iNOS, inflammation, oxidative stress-myeloperoxidase/low-density lipoprotein in rat

The present study aimed to investigate betanin ameliorates isoproterenol-induced AMI through iNOS, inflammation, oxidative stress-myeloperoxidase (MPO)/low-density lipoprotein (LDL) in rat. Cardiovascular diseases CVD is considered as the first killer of human beings. The major pathogenesis of malignant cardiovascular events is chronic heart failure caused by acute myocardial infarction (AMI). Adult male Sprague-Dawley (SD) rat was induced using 100 mg/kg of isoproterenol and used for proving the effect of betanin on AMI. Betanin improves cardiac function and inhibits infarct size in isoproterenol-induced AMI. Next, betanin inhibits inducible nitric oxide synthase (iNOS) and nuclear factor-kappa (NF-κB) protein expressions of isoproterenol-induced AMI. Betanin reduced oxidative damage (such as superoxide dismutase (SOD), methane dicarboxylic aldehyde (MDA), catalase (CAT) and glutathione (GSH)) and Reactive Oxygen Species (ROS) production in isoproterenol-induced AMI. Interesting, betanin weakens the MPO activity and LDL level in isoproterenol-induced AMI. We firstly demonstrated that betanin ameliorates isoproterenol-induced AMI through iNOS, inflammation, oxidative stress-MPO/LDL in rat.