Abstract Title:

p-Coumaric acid attenuates apoptosis in isoproterenol-induced myocardial infarcted rats by inhibiting oxidative stress.

Abstract Source:

Int J Cardiol. 2013 Oct 9 ;168(4):3259-66. Epub 2013 May 16. PMID: 23684599

Abstract Author(s):

P Stanely Mainzen Prince, Abhro Jyoti Roy

Article Affiliation:

P Stanely Mainzen Prince


BACKGROUND: Cardiac apoptosis plays an important role in the pathology of myocardial infarction. The protective effects of p-coumaric acid on cardiac apoptosis were evaluated in isoproterenol induced myocardial infarcted rats.

METHODS: Rats were pretreated with p-coumaric acid (8 mg/kg body weight) daily for a period of 7 days. After pretreatment, isoproterenol (100 mg/kg body weight) was injected subcutaneously into rats at an interval of 24 h for 2 days to induce myocardial infarction. Cardiac diagnostic markers, heart lipid peroxidation, antioxidant system, histopathological changes of the heart and apoptosis were evaluated in isoproterenol induced myocardial infarcted rats.

RESULTS: Isoproterenol induced myocardial infarcted rats showed a significant increase in the levels of serum cardiac diagnostic markers, heart lipid peroxidation products and a significant decrease in the activities/levels of heart antioxidants. Histopathological findings of myocardial infarcted rats revealed marked necrosis and edema. Reverse Transcription Polymerase Chain Reaction study revealed an increase in the myocardial expression of Bax, caspase-8, caspase-9 and Fas genes and a decrease in the myocardial expression of Bcl-2 and Bcl-xL genes. p-Coumaric acid pretreatment showed protective effects on apoptosis by inhibiting oxidative stress. p-Coumaric acid pretreated isoproterenol induced myocardial infarcted heart also confirmed these findings. The possible mechanisms for the protective effects of p-coumaric acid could be attributed to antilipid peroxidative, antioxidant and antiapoptotic properties.

CONCLUSION: Thus, p-coumaric acid protected the myocardial infarcted rat's heart against apoptosis by inhibiting oxidative stress.

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Sayer Ji
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