Epigallocatechin-3-gallate inhibits angiotensin II-induced cardiomyocyte hypertrophy via regulating Hippo signaling pathway in H9c2 rat cardiomyocytes

Acta Biochim Biophys Sin (Shanghai). 2019 Apr 1;51(4):422-430. doi: 10.1093/abbs/gmz018.

Abstract

Angiotensin II (AII) has been well known to induce cardiomyocyte hypertrophy. Epigallocatechin-3-gallate (EGCG) is the main active component of green tea and it has been shown to exhibit strong cardioprotective potential, although the underlying molecular mechanisms remain unclear. In this study, we investigated the role and mechanism of EGCG in preventing AII-induced cardiomyocyte hypertrophy using rat H9c2 cardiomyocytes cells. Reactive oxygen species assay, cell size, and mRNA expression of cardiac hypertrophy markers ANP and BNP were assessed in response to AII treatment. In addition, expression of proteins involved in Hippo signaling pathway were determined by western blot analysis. We found that AII treatment resulted in significant upregulation of ANP and BNP expression levels and increase in H9c2 cell size, which were markedly attenuated by EGCG treatment. Furthermore, our results suggested that EGCG inhibited AII-induced cardiac hypertrophy via regulating the Hippo signaling pathway. Therefore, EGCG may be an effective agent for preventing cardiac hypertrophy.

Keywords: Hippo signaling pathway; angiotensin II; cardiomyocyte hypertrophy; epigallocatechin-3-gallate.

MeSH terms

  • Angiotensin II
  • Animals
  • Atrial Natriuretic Factor / genetics
  • Atrial Natriuretic Factor / metabolism
  • Cardiomegaly / chemically induced
  • Cardiomegaly / genetics
  • Cardiomegaly / prevention & control*
  • Catechin / analogs & derivatives*
  • Catechin / chemistry
  • Catechin / pharmacology
  • Cell Line
  • Gene Expression Regulation / drug effects
  • Molecular Structure
  • Myocytes, Cardiac / cytology
  • Myocytes, Cardiac / drug effects*
  • Myocytes, Cardiac / metabolism
  • Natriuretic Peptide, Brain / genetics
  • Natriuretic Peptide, Brain / metabolism
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism*
  • Rats
  • Reactive Oxygen Species / metabolism
  • Signal Transduction / drug effects*
  • Signal Transduction / genetics

Substances

  • Reactive Oxygen Species
  • Angiotensin II
  • Natriuretic Peptide, Brain
  • Atrial Natriuretic Factor
  • Catechin
  • epigallocatechin gallate
  • Protein Serine-Threonine Kinases