L-Carnitine Protects Cardiac Damage By Reducing Oxidative Stress And Inflammatory Response Via Inhibition Of Tumor Necrosis Factor-Alpha And Interleukin-1beta Against Isoproterenol-Induced Myocardial Infarction

Brief introduction: Myocardial infarction (MI) is a common manifestation of certain cardiac diseases where oxidative stress and fibrosis aggravate the condition markedly. Main objective of the study: Investigation of L-carnitine's cardioprotective roles and mechanism of action in a rat model of MI. Methods: To develop a MI animal model, Isoproterenol (ISO) was administered in male Long Evans rats where animals were divided into five groups (six rats/group). The oxidative stress and antioxidant enzyme activities were determined by different biochemical tests. The real-time PCR was performed to determine the expression of TNF-alpha and Il-1 beta. Histopathological observations by hematoxylin-eosin and Masson trichrome were made to observe the tissue damage and fibrosis in heart and kidney. Significant findings from the study: The ISO-treated rats showed increased levels of troponin I and lipid peroxidation and lower antioxidant enzyme activity in heart and kidney tissues. The levels of TNF-alpha and IL-1 beta were also increased in ISO-rats. Co-administration of L-carnitine with ISO reversed all these parameters. The elevated levels of uric acid and creatinine kinase and ALP, AST and ALT activities in ISO-rats were also significantly reduced by L-carnitine administration. L-carnitine markedly decreased the infiltration of inflammatory cells and improved the tissue architecture in heart and kidney. Control animals did not show any appreciable response upon Lcarnitine administration. Relevant contribution to knowledge: These results suggest that L-carnitine plays a defensive role against cardiac and renal damage in ISO-treated MI rat model via suppressing oxidative stress and increasing antioxidant enzyme functions through inhibition of TNF-alpha and IL-1 beta.