This investigation aimed to investigate whether azilsartan, a drug that acts as both an angiotensin II receptor antagonist and a limited PPAR-γ inhibitor, can prevent AMI in rats that were administered isoproterenol. The study aimed to determine if azilsartan treatment could reverse the hemodynamic, biochemical, and histopathological variations observed in the rat myocardium. The damaging effects of isoproterenol on the heart were evident from the significant reduction in SAP, DAP, and MAP, in addition to in indicators of MI contraction as well as relaxation ( ± LVdP/dtmax) together through a surge in LVEDP, an indicator of pre-load. Additionally, the actions of important enzymes like CK-MB, LDH, along with antioxidant enzymes for example, superoxide dismutase (SOD) and catalase, in adding to the stage of glutathione (GSH), were notably reduced. An elevation in malondialdehyde (MDA) content, a marker of oxidative stress, accompanied this. In this study, rats were pre-treated with different doses of azilsartan (1, 5, and 10 mg/kg bw) orally for 14 days before being induced through isoproterenol-induced myocardial injury. The outcomes of the examination presented that azilsartan had a protecting outcome on the myocardium in this experimentally induced model of myocardial infarction (MI). The treatment with azilsartan improved various parameters, positively impacting the damaging effects caused by isoproterenol (ISO).
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Shirsath et al. (2024) studied this question.
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