P38MAPK抑制剂对小鼠急性水肿型胰腺炎的作用  

The Effect of P38MAPK Inhibitor on Acute Edematous Pancreatitis in Mice

作　　者：俞华芳[1] 樊晓明[1] 蒋淼[1] 范卫[2] 刘娓娓[1] 

机构地区：[1]复旦大学附属金山医院消化科,上海200540 [2]复旦大学附属金山医院中心实验室,上海200540

出　　处：《中国临床医学》2008年第1期82-83,共2页Chinese Journal of Clinical Medicine

基　　金：上海市金山区科委资助项目(项目编号2003-3-4)

摘　　要：目的:探讨P38MAPK抑制剂对急性水肿型胰腺炎的疗效及其机制。方法:雨蛙素建立小鼠水肿型胰腺炎模型,分成对照组、造模组和SB203580治疗组,分别测定血清淀粉酶、血清TNF-α和IL-6,并作胰腺病理评分。结果:SB203580组水肿型胰腺炎的病理病变减轻,血清淀粉酶水平下降,但血清TNF-α与IL-6水平无变化。结论:抑制P38MAPK传导途径能减轻水肿型胰腺炎,但与TNF-α、IL-6无明显关系。Objective：To explore the role of P38MAPK inhibitor on acute expremental cerulein edematous pancreatitis. Methods：Mice were treated with cerulein, arid with or without a specific p38 inhibitor （SB203580）. Serum amylase, TNF-α and IL-6 were detected and pancreas pathologic score was recorded. Results： P38 MARK inhibition with SB203580 ameliorated pancreatitis, redcuing pancreatic edema and amylase level,but not altering the level of TNF-α and IL-6. Conclusion： P38MARK may promote pancreatitis development,its inhibitor ameliorates pancreatitis. But P38 inhibitor did not reduce the level of TNF-α and IL-6, which may mediate pancreatitis.

关 键 词：水肿型胰腺炎 P38丝裂原激活蛋白酶抑制剂 肿瘤坏死因子一a 白介素一6 

分 类 号：R576[医药卫生—消化系统]