P Stanely Mainzen Prince1, Abhro Jyoti Roy. 1. Department of Biochemistry and Biotechnology, Annamalai University, Annamalai Nagar - 608002, Tamil Nadu, India. Electronic address: ps_mainzenprince@yahoo.co.in.
Abstract
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.
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 infarctedrats. 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 infarctedrats. RESULTS:Isoproterenol induced myocardial infarctedrats 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 infarctedrats 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 infarctedrat's heart against apoptosis by inhibiting oxidative stress.
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