首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >EGCG Blocked Phenylephrin-Induced Hypertrophy in H9C2 Cardiomyocytes, by Activating AMPK-Dependent Pathway
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EGCG Blocked Phenylephrin-Induced Hypertrophy in H9C2 Cardiomyocytes, by Activating AMPK-Dependent Pathway

机译:通过激活AMPK依赖性途径,EGCG阻断H9C2心肌细胞中的苯肾上腺素诱导的肥大。

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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.
机译:AMP激活的蛋白激酶(AMPK)是能量代谢的关键调节剂。先前的研究表明,AMPK的激活可通过抑制p70S6激酶(p70S6K)和真核延伸因子2(eEF2)信号通路来抑制心肌肥大。 Epigallocatechin-3-gallate(EGCG)是绿茶中发现的主要多酚,对心血管系统(包括心脏肥大)具有多种保护作用。但是,分子机理尚未得到充分研究。在这项研究中,我们发现EGCG可以显着降低A肾上腺素钠肽(Nppa),脑钠素(BNP)mRNA表达,并减少去氧肾上腺素(PE)刺激的H9C2心肌细胞的细胞表面积。此外,我们表明AMPK在EGCG中激活了H9C2心肌细胞,而AMPK依赖性途径参与了EGCG对心肌肥大的抑制作用。综上所述,我们的发现提供了第一个证据,证明EGCG抗心肌肥大的作用可能归因于其对AMPK依赖性信号通路的激活,这提示EGCG在预防压力超负荷肥大患者心脏重塑中的治疗潜力。

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