Journal
ACTA PHARMACOLOGICA SINICA
Volume 31, Issue 10, Pages 1401-1406Publisher
ACTA PHARMACOLOGICA SINICA
DOI: 10.1038/aps.2010.75
Keywords
angiotensin II; epigallocatechin gallate; endothelial barrier function; mitogen-activated protein kinases; heat-shock protein 27
Funding
- National Natural Science Foundation of China [2006CB910306]
- 111 project [B08007]
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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 mu mol/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) mu mol/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.
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