Epigallocatechin-3 gallate prevents cardiac hypertrophy induced by pressure overload in rats.
- Author:
Jia HAO
1
;
Chan Hyung KIM
;
Tae Sun HA
;
Hee Yul AHN
Author Information
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords: cardiac hypertrophy; EGCG; pressure overload
- MeSH: Animals; Blood Pressure/drug effects; Cardiomegaly/pathology/*prevention & control; Catechin/*analogs & derivatives/pharmacology; Echocardiography; Heart Rate/drug effects; Histocytochemistry; Male; Organ Size/drug effects; Rats; Rats, Sprague-Dawley
- From:Journal of Veterinary Science 2007;8(2):121-129
- CountryRepublic of Korea
- Language:English
- Abstract: Pressure overload diseases, such as valvular stenosis and systemic hypertension, manifest morphologically in patients as cardiac concentric hypertrophy. Prevention of cardiac remodeling due to increased pressure overload is important to reduce morbidity and mortality. Epigallocatechin-3 gallate (EGCG) is a major bioactive polyphenol present in green tea which has been found to be a nitric oxide-mediated vasorelaxant and to be cardioprotective in myocardial ischemia-reperfusion injury. Therefore, we investigated whether EGCG supplementation could reduce in vivo pressure overloadmediated cardiac hypertrophy. Cardiac hypertrophy was induced by suprarenal transverse abdominal aortic constriction (AC) in rats. Three weeks after AC surgery, heart to body weight ratio increased in the AC group by 34% compared to the sham group. EGCG administration suppressed the load-induced increase in heart weight by 69%. Attenuation of cardiac hypertrophy by EGCG was associated with attenuation of the increase in myocyte cell size and fibrosis induced by aortic constriction. Despite abolition of hypertrophy by EGCG, transstenotic pressure gradients did not change. Echocardiogram revealed that increased left ventricular systolic dimensions and deteriorated systolic function were relieved by EGCG. These results suggest that EGCG prevents the development of left ventricular concentric hypertrophy by pressure overload and may be a useful therapeutic modality to prevent cardiac remodeling in patients with pressure overload myocardial diseases.
