Cardioprotective Effects of Ferulic Acid Through Inhibition of Advanced Glycation End Products in Diabetic Rats with Isoproterenol-Induced Myocardial Infarction.

BACKGROUND/OBJECTIVES: Myocardial infarction (MI) and diabetes pose significant health challenges globally, necessitating the development of innovative medication strategies to improve outcomes in affected populations. This research aimed to determine the defensive impact of ferulic acid (FA) against isoproterenol-induced myocardial infarction (MI) in diabetic rats. METHODS: A group of male rats was partitioned into five distinct groups: control group, diabetic group, diabetic + MI, diabetic + MI + 20 mg/kg FA, and diabetic + MI + 40 mg/kg FA. The experimental groups received isoproterenol (ISO) subcutaneously at a dosage of 50 mg/kg body weight for two consecutive days. RESULTS: The outcome was severe cardiac toxicity, as shown by changes in electrocardiogram (ECG) rhythm and a substantial increase in blood cardiac enzymes such as creatinine kinase (CK-MB), cardiac troponin I (cTnI), and lactate dehydrogenase (LDH). Additionally, there was a surge in inflammatory cytokines, like tumor necrosis factor-alpha (TNF-α), and a disruption of the antioxidant system, evidenced by a rise in malondialdehyde (MDA) content. Moreover, there was a rise in cardiac receptor of advanced glycation end products (RAGE). Treatment with FA with escalating dosages of 20 and 40 mg/kg b.w. effectively mitigated changes in serum cardiac enzymes and improved the cellular architecture, which was evaluated by histopathological examination. CONCLUSIONS: In conclusion, in a dose-dependent manner, FA successfully showed a cardioprotective effect against ISO-induced cardiac toxicity in diabetic rats, as shown by the improvement in ECG findings, normalization of serum cardiac biomarkers, and augmentation of the endogenous antioxidant system. Therefore, the aforementioned data indicate that ferulic acid may potentially have a protective effect on MI patients who have diabetes mellitus.