| 19298531 |
Chen DD, Dong YG, Liu D, He JG: Epigallocatechin-3-gallate attenuates cardiac hypertrophy partly via MAPKs signals in hypertensive rats. Clin Exp Pharmacol Physiol. 2009 Mar 2.
1. It has been demonstrated that epigallocatechin-3-gallate (EGCG) inhibits cardiac hypertrophy through its anti-hypertension and anti-oxidative effects. However, the underlying molecular mechanism is not clear yet. 2. In the present study, we tested the hypothesis that EGCG attenuates transaortic abdominal aortic constriction (TAC)-induced ventricular hypertrophy via regulating mitogen-activated protein kinases (MAPK) signal pathways in hypertensive rats. 3. The results showed that the left ventricular myocyte diameter and the expression of atrial natriuretic peptide, brain natriuretic peptide, and beta-myocardial heavy chain were significantly decreased in EGCG treated (50 mg.kg (-1).day (-1), intraperitoneally) TAC group. The levels of reactive oxygen species and malondialdehyde in left ventricle were significantly reduced by EGCG in TCA group. The activities of total superoxide dismutase, catalase, and glutathione peroxidase were increased in TCA group, which were blunted by EGCG treatment. The phosphorylations of ERK2, p38, and JNK1 were significantly increased in left ventricle of EGCG treated TCA rats, accompanied with activations of NF-kappaB and AP-1. The expression of matrix metalloproteinases-9 was significantly upregulated in the left ventricle of TAC rats, which can be inhibited by EGCG treatment. The copy number of mitochondrial DNA and activities of respiratory chain complexes I, III and IV were decreased after TAC, which were reversed in EGCG treated TAC rats. 4. In conclusion, EGCG attenuates TAC-induced ventricular hypertrophy partly through suppression of antioxidant enzymes and regulations of MAPK signals in hypertensive rats. |
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