J Vet Sci.  2007 Jun;8(2):121-129. 10.4142/jvs.2007.8.2.121.

Epigallocatechin-3 gallate prevents cardiac hypertrophy induced by pressure overload in rats

• Hao J
• Kim CH
• Ha TS
• Ahn HY

• KMID: 1089662
• DOI: http://doi.org/10.4142/jvs.2007.8.2.121

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.

Keyword

cardiac hypertrophy; EGCG; pressure overload

MeSH Terms

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

Figure

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  Fig. 1 Experimental design. One day before the operation, rats were randomly treated with EGCG or no drug. EGCG was dissolved in drinking water and the administered solutions were replaced every day for 3 weeks. Hemodynamic and morphologic measurements were performed at for various time intervals after abdominal aortic constriction (AC). Cardiac function was measured after 8 weeks of AC.

• 

  Fig. 2 Inhibition of pressure overload induced cardiac hypertrophy in vivo by EGCG. A, Heart wet weight was normalized to body weight in each rat as an index of cardiac hypertrophy. Heart weight to body weight ratio was attenuated in a dose-dependent manner by EGCG after 3 weeks of aortic constriction (AC). B, Liver weight to body weight ratio. #P < 0.001 compared with sham, n = 8; *P < 0.001 compared with AC, n ≥ 6. C, Representative hearts of rats treated with AC or AC + 0.04% EGCG for 3 weeks. scale = 1 mm.

• 

  Fig. 3 Effect of ECGC on myocyte cell area and cardiac fibrosis. A, heart tissues. H&E stain. bar = 50 µm. B, Cardiomyocyte cross sectional area was decreased in the EGCG-treated group after 3 weeks of aortic constriction (AC). #P < 0.001 compared with sham, *P < 0.001 compared with AC. C, Inhibition of perivascular fibrosis in vivo by EGCG. Cason's stain. bar = 200 µm.

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  Fig. 4 Inhibition of cardiac hypertrophy in vivo by EGCG at various time intervals with pressure overload. #P < 0.05 compared with sham, *P < 0.001 compared with AC (n ≥ 11).

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  Fig. 5 Representative M-mode echocardiograms after 8 weeks of aortic constriction (AC). Quantitative data are shown in Table 2. Concentric cardiac remodeling was observed in the AC group.

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