Literature DB >> 19263074

Green tea extract protects rats against myocardial infarction associated with left anterior descending coronary artery ligation.

Shih-Rong Hsieh1, Dan-Chin Tsai, Jan-Yow Chen, Sen-Wei Tsai, Ying-Ming Liou.   

Abstract

There is increasing evidence that green tea polyphenols can protect against myocardial damage. Recently, we showed that they bind to cardiac troponin C and alter myofilament Ca(2+) sensitivity in cardiac muscle. In the present study, we examined whether green tea extract (GTE) could prevent the progressive remodeling seen in ischemic myocardium and improve cardiac function by modulation of the contractile apparatus utilizing a myocardial infarction (MI) model in the rat involving ligation of the left anterior descending branch. Using this model, severe myocardial injury was found, including altered cardiac performance and the appearance of extensive fibrosis and left ventricular (LV) enlargement. Supplementation with 400 mg/kg/day of GTE for 4, 18, or 46 days had beneficial effects in preventing the hemodynamic changes. Histopathological studies showed that GTE attenuated the progressive remodeling seen after myocardial injury. Echocardiography confirmed that GTE prevented LV enlargement and improved LV performance in post-MI rats. In addition, we showed that GTE supplementation for 18 or 46 days increased the myofilament Ca(2+) sensitivity of the ischemic myocardium in post-MI rats. These results validate the novel action of green tea polyphenols in protecting against myocardial damage and enhancing cardiac contractility by modulating myofilament Ca(2+) sensitivity in post-MI rats.

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Year:  2009        PMID: 19263074     DOI: 10.1007/s00424-009-0655-1

Source DB:  PubMed          Journal:  Pflugers Arch        ISSN: 0031-6768            Impact factor:   3.657


  48 in total

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7.  The counteracting effects of (-)-Epigallocatechin-3-Gallate on the immobilization stress-induced adverse reactions in rat pancreas.

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8.  Molecular identification for epigallocatechin-3-gallate-mediated antioxidant intervention on the H2O2-induced oxidative stress in H9c2 rat cardiomyoblasts.

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  9 in total

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