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Apigenin Attenuates β-Receptor-Stimulated Myocardial Injury Via Safeguarding Cardiac Functions and Escalation of Antioxidant Defence System

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Abstract

Apigenin (AP) is a flavone in dietary flavonoids reported as strong antioxidant and elite modulator of PPARγ. The current study evaluated the consequence of AP in isoproterenol (ISO)-induced oxidative stress and myocardial infarction during β-adrenergic receptor stimulus in rats by persistent hemodynamic, biochemical and histopathological changes. Rats received AP (25, 50 and 75 mg/kg/day) or vehicle i.p. for 14 days and ISO (100 mg/kg, s.c.) on 13th and 14th days for initiation of cardiotoxicity. ISO-treated rats showed evidence of significant dwindle in systolic and diastolic arterial pressures, maximal positive rate of developed left ventricular pressure. In totting up, a noteworthy diminution in activities of creatine kinase-MB isoenzyme, reduced glutathione, superoxide dismutase, catalase and level along with rise in malondialdehyde content were observed. The shielding function of AP on isoproterenol-induced myocardial damage was observed by attenuating all the endogenous parameters and the membrane-bound enzymes. It was confirmed by histopathological examinations. The effect of AP at the doses of 50 and 75 mg/kg showed added apparent than at the dose of 25 mg/kg. Current study thus provides confirmation for protective effects of AP on myocardium in experimentally induced myocardial infarction.

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Acknowledgments

The authors gratefully acknowledge the financial support received under Young Scientist Research Scheme (File no. SB/YS/LS-114/2013) of Science and Engineering Research Board (SERB), Department of Science and Technology, New Delhi, India.

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  1. Department of Pharmacology, R. C. Patel Institute of Pharmaceutical Education and Research, Shirpur, Dist. Dhule, Maharashtra, India

    Chhabildas C. Buwa, Umesh B. Mahajan, Chandragouda R. Patil & Sameer N. Goyal

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Buwa, C.C., Mahajan, U.B., Patil, C.R. et al. Apigenin Attenuates β-Receptor-Stimulated Myocardial Injury Via Safeguarding Cardiac Functions and Escalation of Antioxidant Defence System. Cardiovasc Toxicol 16, 286–297 (2016). https://doi.org/10.1007/s12012-015-9336-9

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