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目的:研究P38丝裂原活化蛋白激酶(P38MAPK)对重症急性胰腺炎(SAP)大鼠海马神经元环氧合酶-2(COX-2)和前列腺素E2(PGE2)表达的调控作用。方法:雄性健康SD大鼠36只,体重220~260 g,随机分为3组。SAP模型组:采用向胰胆管内注入5%牛磺胆酸钠(2 mg/kg)的方法制备SAP动物模型;抑制剂组:SAP建模成功5 min后,大鼠尾静脉注射P38MAPK抑制剂SB203580(10 mg/kg);对照组:行剖腹术翻动胰腺和十二指肠后缝合腹腔。各组大鼠分别于术后24 h,用Nissl染色和免疫组化法观察脑组织病理改变的情况,用Western Blot检测脑组织中p-P38蛋白、COX-2和PGE2的表达情况。结果:模型组大鼠海马CA1区局部锥体细胞缺失,p-P38、COX-2和PGE2阳性细胞数明显增加(P<0.01),且相应蛋白表达显著升高(P<0.01);SB203580处理组以上变化明显减轻或不明显(P<0.01)。结论:P38MAPK对实验SAP大鼠海马COX-2和PGE2表达具有显著调控作用,而P38MAPK抑制剂SB203580则对SAP大鼠海马神经元具有一定保护作用。
AIM: To investigate the regulatory effect of P38 mitogen activated protein kinase (P38MAPK) on the expression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) in the hippocampus of rats with severe acute pancreatitis (SAP). Methods: Thirty-six male healthy SD rats weighing 220-260 g were randomly divided into three groups. SAP model group: SAP animal model was established by injecting 5% sodium taurocholate (2 mg / kg) into pancreaticobiliary ducts; inhibitor group: P38MAPK inhibitor SB203580 (10 mg / kg); control group: The abdominal cavity was sutured after laparotomy and pancreas were performed by laparotomy. The changes of brain pathology were observed by Nissl staining and immunohistochemistry 24 hours after operation. The expression of p-P38 protein, COX-2 and PGE2 in brain tissue were detected by Western Blot. Results: The number of pyramidal neurons in hippocampal CA1 region of model group was significantly decreased (P <0.01), and the expression of p-P38, COX-2 and PGE2 was significantly increased (P <0.01) The above changes were significantly reduced or insignificant (P <0.01). CONCLUSION: P38MAPK plays a significant role in the regulation of COX-2 and PGE2 expression in hippocampus of SAP rats, while P38MAPK inhibitor SB203580 has a protective effect on hippocampal neurons of SAP rats.