急性重症胰腺炎大鼠P38丝裂原活化蛋白激酶通路对海马神经元环氧化酶-2和前列腺素E2表达的调控  

Regulation of P38MAPK pathway on the cyclooxygenase-2 and prostaglandin E2 expression in hippocampal neurons in rat model of severe acute pancreatitis

作　　者：蒙国光[1] 郑国利[1] 朱世纯 张宇新[2] 

机构地区：[1]唐山市丰润区人民医院普外科 [2]河北联合大学解剖学教研室,唐山063000

出　　处：《解剖学杂志》2015年第5期559-559,共4页Chinese Journal of Anatomy

基　　金：河北省唐山市科学技术研究与发展计划项目(111302069a)

摘　　要：目的:研究在急性重症胰腺炎(SAP)大鼠模型中,P38丝裂原活化蛋白激酶(P38MAPK)通路对于海马CA1区神经元环氧化酶-2(COX-2)和前列腺素E2(PGE2)表达的影响.方法:随机将SD大鼠分为SAP模型组、SB203580抑制剂组和对照组.采用Nissl染色、免疫组织化学显色、免疫印迹,观察每组大鼠海马CA1区p-P38、COX-2以及PGE2的表达变化和SB203580对上述指标变化的影响.结果:SAP模型组海马CA1区p-P38、COX-2、PGE2阳性神经元的数量较对照组显著增加;SB203580抑制剂组与SAP模型组比较,海马CA1区p-P38、COX-2、PGE2阳性神经元的数量明显减少.结论:P38MAPK通路对SAP大鼠模型海马COX-2和PGE2表达可能有重要调控作用,SB203580对SAP大鼠海马神经元具有保护作用.Objective:To investigate the effect of P38 mitogen-activated protein kinase(P38MAPK) pathway on the expression of inducible cyclooxygenase-2(COX-2) and prostaglandin E2(PGE2) in hippocampal neurons of the rats model of severe acute pancreatitis(SAP).Methods:Healthy male Spraque-Dawley rats were randomly divided into model group,inhibitor group and control group.By Nissl’s staining,immunohistochemistry and Western blotting,p-P38,COX-2 and PGE2 were detected to observe the changes of positive cell numbers and their changes after being treated with SB203580 in the hippocampal CAl.Results:The number of p-P38,COX-2,PGE2 immunoreactive cells increased markedly in the hippocampal CAl compared with the control group.In the treatment group with SB203580,the number of p-P38,COX-2,PGE2 immunoreactive cells was reduced significantly as compared with the model group(P<0.05).Conclusion:In the rat model of SAP,P38 MAPK pathway regulates the expression of COX-2 and PGE2 in hippocampus,and SB203580 is neuroprotective to the neurons of SAP rat model.

关 键 词：急性重症胰腺炎 海马 P38丝裂原活化蛋白激酶 环氧化酶-2 前列腺素E2 

分 类 号：R657.51[医药卫生—外科学]