大黄素对重症急性胰腺炎肠黏膜屏障的保护作用及机制  

Protective roles of Emodin in the intestinal mucosal layer of rats with severe acute pancreatitis

作　　者：陈霞[1] 赵宏贤 王巧稚 李昌平[1] 

机构地区：[1]泸州医学院附属医院消化内科,646000 [2]四川医科大学组织胚胎学教研室

出　　处：《天津医药》2015年第12期1398-1400,共3页Tianjin Medical Journal

基　　金：四川省卫生厅科研项目(130369)

摘　　要：目的从细胞凋亡方面,探讨大黄素对重症急性胰腺炎(SAP)肠黏膜功能障碍的保护作用及相关作用机制。方法 SD大鼠30只,按随机数字表法分为假手术组、SAP组和大黄素组。采用胰管逆行注射3%牛磺胆酸钠溶液制作SAP模型,大黄素组制作SAP模型1 h后给予大黄素25 mg/kg腹腔注射,2 h后重复1次。TUNEL法检测回肠黏膜细胞凋亡;免疫组化法检测回肠黏膜细胞GRP78蛋白表达。结果与假手术组相比,SAP组大鼠肠黏膜细胞凋亡及GRP78蛋白表达明显增加(P<0.05);与SAP组相比较,大黄素组大鼠肠黏膜细胞凋亡减少(P<0.05),GRP78蛋白表达差异无统计学意义(P>0.05)。结论大黄素可减少SAP时的肠黏膜细胞凋亡,保护肠黏膜屏障,但这种保护作用似乎并未涉及到内质网应激途径。Objective To explore the protective roles of Emodin in the intestinal mucosal lay of rats with severe acute pancreatitis （SAP） and its mechanism. Methods SD rats （n=30） were divided into 3 groups： sham operation group, SAP group and Emodin group （SAP rats treated with Emodin）. The SAP rat models were established via retrograde injection of 3%sodium taurocholate to pancreatic duct. Rats in Emodin group were peritoneally injected with Emodin （2.5 mg/100 g） at both 1 hour and 3 hour after sodium taurocholate injection. Apoptosis of intestinal epithelial cell was detected by TUNEL analysis. The expression of glucose-regulated protein78 （GRP78） protein was assessed by immunohistochemistry. Results Compared with sham operation group, apoptosis in intestinal epithelial cells and the expression of GRP78 protein were increased significantly in SAP group（P〈0.05）. Emodin treatment reduced AP-induced mucosal intestinal epithelial cell apoptosis （P〈0.05）. But there is no significant difference of GRP78 expression between SAP group and Emodin group（P〉0.05）. Conclusion Emodin has a protective effect on intestinal layer in rats with SAP through inhibiting intestinal epithelial cell apoptosis. However, ER stress is not likely to be involved in this protective effect.

关 键 词：胰腺炎 急性坏死性 急性病 肠黏膜 大黄素 细胞凋亡 大鼠 Sprague—Dawley 症急性胰腺炎 葡萄 糖调节蛋白78 

分 类 号：R576.1[医药卫生—消化系统]