The study on the mechanim of clopidogrel in human gastric epithelial GES-1 cell line injury
10.3760/cma.j.issn.0254-1432.2011.11.002
- VernacularTitle:氯吡格雷对人胃黏膜上皮细胞损伤机制的研究
- Author:
Zongdan JIANG
;
Zhenyu ZHANG
;
Zhibing WANG
;
Gongyu ZHANG
;
Bangshun HE
;
Shukui WANG
;
Jinsong WANG
;
Wenbin HUANG
- Publication Type:Journal Article
- Keywords:
Ticlopidine;
Signal transduction;
Gastric mucosa;
Epithelial cells;
Cell line
- From:
Chinese Journal of Digestion
2011;31(11):724-728
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore the mechanism of clopidogrel in human gastric epithelial cell line (GES-1) injury.MethodsSet up GES-1 cells monolayer culture model.Then the GES-1 cells were divided into negative control group,U0126 intervented group,clopidogrel intervented group and combined intervented group (U0t26 treated firstly then clopidogrel intervented).The cell proliferation and apoptosis in each group was examined by methyl thiazolyl tetrazolium (MTT) assay and Flow cytometry.TheexpressionofphosphorylatedERK1/2ineachgroupwasdetectedby immunocytochemistry method,and the expression quantity of phosphorylated ERK1/2 in each group was measured by western blot.ResultsThe result of MTT assay showed that compared with negative control group,the proliferation of GES-1 cells was inhibited in U0126 group,clopidogrel group and combined intervented group,and the inhibition percentage was 21.8％ ±2.7％,46.3％ ± 3.4％ and 82.9 ％ ± 0.8 ％ respectively ( F=615.556,P =0.000 ).The result of immunocytochemistry indicated that the expression of p-ERK in U0126 group,Clopidogrel group and combined intervented group decreased compared with negative control group,which was 10.80±1.64,7.20± 1.64,4.40±0.89and 1.40±0.55 respecitively (F=49.426,P=0.000).The result of western blot and immunocytochemistry was of the same trend.Conclusion In GES-1 cell model,clopidogrel may injureGES-1 cells through MAPK/EPK signal transduction pathway.
