EGCG Blocked Phenylephrin-Induced Hypertrophy in H9C2 Cardiomyocytes, by Activating AMPK-Dependent Pathway.
10.4196/kjpp.2015.19.3.203
- Author:
Yi CAI
1
;
Li ZHAO
;
Yuan QIN
;
Xiao Qian WU
Author Information
1. Guangzhou Research Institute of Snake Venom, China. yicaisysu@163.com
- Publication Type:Original Article
- Keywords:
AMP-activated protein kinase;
Epigallocatechin-3-gallate;
H9C2 cardiomyocytes;
Phenylephrine
- MeSH:
AMP-Activated Protein Kinases;
Brain;
Cardiomegaly;
Cardiovascular System;
Energy Metabolism;
Humans;
Hypertrophy*;
Myocytes, Cardiac*;
Natriuretic Peptides;
Phenylephrine;
Phosphotransferases;
RNA, Messenger;
Tea
- From:The Korean Journal of Physiology and Pharmacology
2015;19(3):203-210
- CountryRepublic of Korea
- Language:English
-
Abstract:
AMP-activated protein kinase (AMPK) is a key regulator of energy metabolism. Previous studies have shown that activation of AMPK results in suppression of cardiac myocyte hypertrophy via inhibition of the p70S6 kinase (p70S6K) and eukaryotic elongation factor-2 (eEF2) signaling pathways. Epigallocatechin-3-gallate (EGCG), the major polyphenol found in green tea, possesses multiple protective effects on the cardiovascular system including cardiac hypertrophy. However, the molecular mechanisms has not been well investigated. In this study, we found that EGCG could significantly reduce natriuretic peptides type A (Nppa), brain natriuretic polypeptide (BNP) mRNA expression and decrease cell surface area in H9C2 cardiomyocytes stimulated with phenylephrine (PE). Moreover, we showed that AMPK is activated in H9C2 cardiomyocytes by EGCG, and AMPK-dependent pathway participates in the inhibitory effects of EGCG on cardiac hypertrophy. Taken together, our findings provide the first evidence that the effect of EGCG against cardiac hypertrophy may be attributed to its activation on AMPK-dependent signaling pathway, suggesting the therapeutic potential of EGCG on the prevention of cardiac remodeling in patients with pressure overload hypertrophy.
