CAJ | 학술논문

目的研究p38 MAPK在胰蛋白酶(trypsin)诱导食管黏膜上皮细胞炎症反应中的机制.方法原代培养食管黏膜上皮细胞,使用胰蛋白酶进行刺激,观察p38 MAPK磷酸化程度;给予p38 MAPK抑制剂SB203580(1、10 μmol/L)进行干预治疗,观察炎症相关指标的变化.结果胰蛋白酶刺激剂量依赖地增加了p38 MAPK磷酸化,提示胰蛋白酶激活了食管黏膜上皮细胞中的p38MAPK通路;SB203580治疗抑制了胰蛋白酶诱导的炎症因子白介素8(IL-8)、环氧酶2(COX2)、肿瘤坏死因子α(TNFα)的mRNA表达水平,同时抑制了胰蛋白酶诱导的食管上皮细胞中诱导性一氧化氮合酶(iNOS)的蛋白表达和细胞中一氧化氮(NO)的生成.结论 p38 MAPK通过调节IL-8、COX2、TNFα、iNOS等炎症相关因子参与了胰蛋白酶诱导的食管黏膜上皮损伤.
목적 연구p38 MAPK재이단백매(trypsin)유도식관점막상피세포염증반응중적궤제.방법 원대배양식관점막상피세포,사용이단백매진행자격,관찰p38 MAPK린산화정도;급여p38 MAPK억제제SB203580(1、10 μmol/L)진행간예치료,관찰염증상관지표적변화.결과 이단백매자격제량의뢰지증가료p38 MAPK린산화,제시이단백매격활료식관점막상피세포중적p38MAPK통로;SB203580치료억제료이단백매유도적염증인자백개소8(IL-8)、배양매2(COX2)、종류배사인자α(TNFα)적mRNA표체수평,동시억제료이단백매유도적식관상피세포중유도성일양화담합매(iNOS)적단백표체화세포중일양화담(NO)적생성.결론 p38 MAPK통과조절IL-8、COX2、TNFα、iNOS등염증상관인자삼여료이단백매유도적식관점막상피손상.
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.