p38MAPK信号通路在雨蛙素诱导的胰腺AR42J细胞炎症反应中的作用

Role of p38 MAPK signaling pathway in inflammatory effects on cerulein-induced pancreatic cells

目的:探讨p38 MAPK信号通路在急性胰腺炎体外模型中的作用。方法:AR42J细胞随机分为3组:正常对照组、雨蛙素组(10-8mol/L雨蛙素)和SB203580组(10μmol/L SB203580+10-8mol/L雨蛙素)。于3h收集细胞,检测淀粉酶分泌率;免疫荧光染色观察p-p38 MAPK核移位;Western blotting印迹检测p-p38 MAPK和TNF-α蛋白表达;EMSA检测NF-κB活性。结果:与正常对照组比较,雨蛙素组淀粉酶分泌率和TNF-α蛋白水平增高(P<0.01),p-p38 MAPK表达及NF-κB活性表达增加(P<0.01);免疫荧光示雨蛙素组p-p38MAPK发生了核移位。而与雨蛙素组相比,SB203580组明显降低淀粉酶分泌率和TNF-α蛋白表达(P<0.01),p-p38 MAPK和NF-κB的活性表达也下降(P<0.05);SB203580还抑制了p-p38 MAPK核移位。结论:p38MAPK通路参与了胰腺细胞内的炎症反应,其机制可能涉及NF-κB通路的活化。

AIM： To investigate the effect of p38 MAPK signal pathway on cerulein-treated pancreatic acinar AR42J cells.METHODS： AR42J cells were divided into control group,cerulein group（treated with 10-8 mol/L of cerulein）,and SB203580 group（treated with 10 μmol/L of SB203580 and 10-8mol/L of cerulein）.The cells were harvested 3 h after treatment. Secretion rate of amylase was measured.The translocation of p-p38 MAPK to nuclei was imaged by immunofluorescence.The protein expression levels of p-p38 MAPK and TNF-α were detected by Western blotting.The activation of NF-κB was measured by electrophoretic mobility assay.RESULTS： Compared with control group,cerulein resulted in increases in the secretion rate of amylase and protein level of TNF-α（P0.01）,as well as the expression levels of p-p38 MAPK and NF-κB（P0.01）.Cerulein induced nuclear translocation of p-p38 MAPK.Compared with cerulein group,the secretion rate of amylase and protein level of TNF-α in SB203580 group decreased significantly（P0.01）.The expression of p-p38 MAPK and NF-κB also decreased greatly（P0.05）.Nuclear translocation of p-p38 MAPK was inhibited by SB203580.CONCLUSION： The p38 MAPK pathway involves in cerulein-induced pancreatic inflammatory response via regulating NF-κB.