Hardik Koria
Research Scholar, Gujarat Technological University, Ahmedabad - 382424, Gujarat, India; Department of Pharmacology, Ramanbhai Patel College of Pharmacy, Charotar University of Science and Technology (CHARUSAT), CHARUSAT campus, Changa - 388421, Gujarat, India
Anita Mehta
Department of Pharmacology, Anand Pharmacy College, Anand - 388001, Gujarat, India
ABSTRACT
Introduction: Myocardial infarction (MI) is a major cause of cardiac morbidity and mortality, driven by oxidative stress, inflammation, and cell death. Heme oxygenase-1 (HO-1), a stress-responsive enzyme, is known for its cytoprotective and antioxidant properties. Objective: The objective of this study was to investigate the cardioprotective potential of HO-1 induction by hemin and to explore the involvement of the PI3K signalling pathway in a rat model of isoproterenol-induced myocardial infarction. Methods: Rats were divided into three groups: Normal control., Disease control, and Hemin-treated. ECG parameters, myocardial injury markers (CK-MB and LDH), oxidative stress (MDA), antioxidant enzyme activities (SOD, catalase), HO-1 and PI3K activity, and histopathological changes were evaluated to assess the effect of hemin-induced HO-1 activation. Results: Isoproterenol administration induced significant myocardial injury, as evident by ST-segment elevation, pathological Q-waves, increased CK-MB and LDH levels, elevated MDA, suppressed SOD and catalase activities, and histopathological changes. Hemin treatment significantly attenuated theses pathological changes, improved antioxidant defenses, and preserved cardiac tissue architecture. Hemin induced HO-1 activation offers significant cardioprotection against isoproterenol-induced myocardial injury. HO-1 activity and PI3K signalling were significantly enhanced in the hemin-treated group, suggesting and association between HO-1 induction and PI3K pathway activation. Conclusion: Hemin induced HO-1 induction appears to confer cardioprotection, possibly mediated by PI3K signalling.
Keywords: Heme Oxygenase-1, Hemin, Myocardial Infarction, Cardioprotection, Oxidative Stress, Isoproterenol and PI3K Signaling.
