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Epigallocatechin gallate inhibits angiotensin II-induced endothelial barrier dysfunction via inhibition of the p38 MAPK/HSP27 pathway.

Abstract：

AIM:To investigate the effect of epigallocatechin gallate (EGCG) on angiotensin II (Ang II)-induced stress fiber formation and hyperpermeability in endothelial cells. METHODS:Human umbilical vein endothelial cells (HUVECs) were treated with Ang II in the absence or presence of EGCG or mitogen-activated protein kinases (MAPKs) inhibitors. The resulting stress fibers were stained with rhodamine-phalloidin and examined using confocal microscopy. The permeability of the endothelium was tested with fluorescein-isothiocyanate labeled bovine serum albumin (FITC-BSA), and the phosphorylation levels of several proteins were determined using Western blot analysis. RESULTS:Ang II (1-100 nmol/L) treatment markedly provoked stress fiber formation and hyperpermeability in HUVECs in a time- and dose-dependent manner. These effects were abolished by pretreatment with the p38 MAPK inhibitor SB203580 10 μmol/L, indicating that the Ang II-induced endothelial barrier dysfunction was via activation of the p38 MAPK/HSP27 pathway. Furthermore, treatment with EGCG (5-25) μmol/L inhibited Ang II-induced activation of the p38 MAPK/HSP27 pathway, thereby reducing endothelial stress fiber formation and hyperpermeability. CONCLUSION:Our data demonstrate that EGCG inhibits Ang II-induced endothelial stress fiber formation and hyperpermeability via inactivation of p38 MAPK/HSP27 pathway, and suggest that EGCG may protect against endothelial barrier dysfunction and injury.

journal_name

Acta Pharmacol Sin

journal_title

Acta pharmacologica Sinica

authors

Yang D,Liu J,Tian C,Zeng Y,Zheng YH,Fang Q,Li HH

doi

10.1038/aps.2010.75

subject

Has Abstract

pub_date

2010-10-01 00:00:00

pages

1401-6

issue

10

eissn

1671-4083

issn

1745-7254

pii

aps201075

journal_volume

31

pub_type

杂志文章

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