Assessment of tumor necrosis factor alpha in isoproterenol-induced myocadial infarction

Abstract

Introduction: Acute myocardial infarction (AMI) is a major cause of death and disability worldwide. During myocardial infarction injury, inflammatory immune response occurs in infracted myocardium and neighboring tissues. This immuneresponse manifests as an acute necrosis, hypertrophy, and apoptosis of cardiomyocytes. Tumor necrosis factor-alpha (TNF-α) modulates a series of biological processes, such as the mediation of host defenses against the growth of neoplastic cells, increased expression of antigens of major histocompatibility complex class I, the development of cachexia, states of shock, and is an effector molecule in various inflammatory processes. Recent studies showed that TNF-α is a key regulating factor in the inflammatory reaction, that acts as a mediator in the inflammatory immune response and myocardial repair.