The mechanism of p38 MAPK action in trypsin-induced inflammatory reaction of esophageal mucosal epithelial cells
10.3760/cma.j.issn.1008-1372.2015.05.009
- VernacularTitle:p38MAPK参与胰蛋白酶诱导的食管上皮细胞炎症
- Author:
Gang LIU
;
Ling ZHANG
;
Xiaojun GUO
;
Guixiang LI
;
Duowu ZOU
- Publication Type:Journal Article
- Keywords:
p38 Mitogen-activated protein kinases/AI/PD/BI;
Trypsin/AE;
Esophagus/PA/ME/DE;
Mucous membrane/PA/ME/DE
- From:
Journal of Chinese Physician
2015;17(5):671-674
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of p38 MAPK in the trypsin-induced injury in human esophageal epithelial cells.Methods Primary cultured human esophageal epithelial cells were stimulated with trypsin (20,40,and 80 μg/ml) for4 hours,phosphorylation of p38 MAPK was evaluated by Western blotting.Primary cultured human esophageal epithelial cells were stimulated with trypsin (40 μg/ml) and treated with p38 MAPK inhibitor (SB203580,1 and 10 μmol/L) simultaneously.Four hours later,the cells were collected for analysis.Results Western blotting results revealed that stimulation with trypsin enhanced phosphorylation of p38 MAPK,indicating that trypsin activated p38 MAPK in esophageal epithelial cells.SB203580 treatment suppressed trypsin-induced expression of pro-inflammatory cytokines including interleukin-8 (IL-8),cyclooxygenase 2 (COX2),and tumor necrosis factor alpha (TNFcα).Finally,SB203580 treatment suppressed trypsin-induced upregulation of protein expression of inducible nitric oxide synthase (iNOS),and subsequently reduced nitric oxide (NO) levels.Conclusions The regulation of p38 MAPK was involved in the trypsin-induced injury in esophageal epithelial cells.
