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Int. J. Mol. Sci. 2017, 18(4), 756; doi:10.3390/ijms18040756

The Protective Effect of Apigenin on Myocardial Injury in Diabetic Rats mediating Activation of the PPAR-γ Pathway

1
Department of Pharmacology, R. C. Patel Institute of Pharmaceutical Education and Research, Shirpur, Maharashtra 425405, India
2
Department of Pharmacology, Cardiovascular Research Laboratory, All India Institute of Medical Sciences, New Delhi 110029, India
3
Department of Pharmaceutics and Quality Assurance, R. C. Patel Institute of Pharmaceutical Education and Research, Shirpur, Maharashtra 425405, India
4
Department of Pharmacology and Therapeutics, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box, 17666 Al Ain, Abu Dhabi, UAE
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Academic Editor: Rosa M. Lamuela-Raventós
Received: 28 January 2017 / Revised: 25 March 2017 / Accepted: 29 March 2017 / Published: 4 April 2017
(This article belongs to the Section Bioactives and Nutraceuticals)
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Abstract

We substantiated the role of peroxisome proliferator-activated receptor-γ (PPAR-γ) activation in the protective effect of apigenin against the myocardial infarction (MI) in diabetic rats. Diabetes was induced by intraperitoneal administration of a single dose of streptozotocin (55 mg/kg). The study groups included diabetic rats receiving vehicle, apigenin (75 mg/kg/day, orally), GW9662 (1 mg/kg/day, intraperitoneally), and a combination of apigenin and GW9662 for 14 days. The MI was induced in all the study groups except the diabetic control group by subcutaneous injection of 100 mg/kg/day of isoproterenol on the two terminal days. The diabetes and isoproterenol-induced MI was evident as a reduction in the maximal positive and negative rate of developed left ventricular pressure and an increase in the left ventricular end-diastolic pressure. The activities of creatine kinase on myocardial bundle (CK-MB) and lactate dehydrogenase (LDH) were also reduced. Apigenin treatment prevented the hemodynamic perturbations, restored the left ventricular function and reinstated a balanced redox status. It protected rats against an MI by attenuating myonecrosis, edema, cell death, and oxidative stress. GW9662, a PPAR-γ antagonist reversed the myocardial protection conferred by apigenin. Further, an increase in the PPAR-γ expression in the myocardium of the rats receiving apigenin reinforces the role of PPAR-γ pathway activation in the cardioprotective effects of apigenin. View Full-Text
Keywords: apigenin; streptozotocin; myocardial infarction; diabetic cardiac complications; PPAR-γ apigenin; streptozotocin; myocardial infarction; diabetic cardiac complications; PPAR-γ
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MDPI and ACS Style

Mahajan, U.B.; Chandrayan, G.; Patil, C.R.; Arya, D.S.; Suchal, K.; Agrawal, Y.O.; Ojha, S.; Goyal, S.N. The Protective Effect of Apigenin on Myocardial Injury in Diabetic Rats mediating Activation of the PPAR-γ Pathway. Int. J. Mol. Sci. 2017, 18, 756.

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