Attenuated expression of the tight junction proteins is involved in clopidogrel-induced gastric injury through p38 MAPK activation

Article ID	Journal	Published Year	Pages	File Type
5859389	Toxicology	2013	8 Pages	PDF

Abstract

âº Clopidogrel suppressed GES-1 cell viability in a concentration- and time-dependent manner. âº Clopidogrel significantly increased dextran permeability, reduced occludin and ZO-1 expression, and induced cell apoptosis. âº Clopidogrel activated p38 MAPK signaling pathway. âº Activation of p38 activity was involved in clopidogrel-induced increase in gastric epithelial cells permeability and disruption of TJ.

Keywords

PBS GES-1 MVEC p38 MAPK inhibitor JNK inhibitor ZO-1 MDCK p38 HBSS DAPI ERK IC50 FITC Jnk 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide 4′,6-diamidino-2-phenylindole c-Jun N-terminal kinase DMSO MAPK MTT p38 MAPK Gastric injury Tight junction Gastrointestinal Dimethyl sulfoxide Microvascular endothelial cells Toxicology Adverse drug reaction Phosphate buffered saline fluorescein isothiocyanate Hank's balanced salt solution JAM Zona occludens 1 Erk inhibitor Tight junction protein p38 mitogen-activated protein kinases clopidogrel extracellular signal-regulated kinase mitogen-activated protein kinases