Possible molecular basis of cardioprotective effects of green tea
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Clinical data suggest that people who use green tea have a lower cardiovascular risk. However, the exact mechanisms of these cardioprotective effects are unknown. We know that STAT1 plays a critical role in promoting apoptotic cell death and STAT3 may antagonise STAT1 and protect cardiac myocytes from ischaemia/reperfusion (I/R) injury. More recently it has been shown that specific molecules such as epigallocatechin-3-gallate (EGCG), which is present in green tea extract (GTE), have antioxidant properties. Considering that: (i) oxygen free radicals (OFR) are produced during myocardial I/R insult and (ii) OFR are responsible for reperfusion cardiac damage, we therefore investigated whether chronic administration per os of GTE reduced I/R damage in the Langendorff perfused isolated rat heart. In addition we evaluated myocardial content of STAT1 and STAT3 and degree of apoptosis. In Sprague-Dawley isolated hearts, GTE reduced the ischaemic mechanical insult, prolonged STAT3 activation/phosphorylation and reduced STAT1 activation with consequent less cell apoptosis. These results show that chronic treatment with GTE protects the heart from I/R injury. Activation of prosurvival STAT3 over the pro-apoptotic STAT1 could be one of the molecular mechanisms involved in green tea-mediated cardiopretection.
KeywordsGreen tea Heart Ischaemia Reperfusion Apoptosis
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