天津医药

天津医药 ›› 2015, Vol. 43 ›› Issue (12): 1398-1400.doi: 10.11958/j.issn.0253-9896.2015.12.014

• 实验研究 • 上一篇    下一篇

大黄素对重症急性胰腺炎肠黏膜屏障的保护作用及机制

陈霞1，赵宏贤2，王巧稚2，李昌平1   

  1. 1 泸州医学院附属医院消化内科（邮编646000）；2 四川医科大学组织胚胎学教研室
  • 收稿日期:2015-03-30 修回日期:2015-08-07 出版日期:2015-12-15 发布日期:2015-12-11
  • 作者简介:陈霞（1978），女，副主任医师，硕士，主要从事肠黏膜屏障方面研究
  • 基金资助:
    四川省卫生厅科研项目（130369）

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

CHEN Xia1, ZHAO Hongxian2, WANG Qiaozhi2, LI Changping1   

  1. 1 Department of Gastroenterology of Affiliated hospital, Luzhou 646000, China; 2 Department of Histology and Embryology, Sichuan Medical University
  • Received:2015-03-30 Revised:2015-08-07 Published:2015-12-15 Online:2015-12-11

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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。

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, 重症急性胰腺炎, 葡萄糖调节蛋白78

Abstract: 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 analy⁃ sis. The expression of glucose-regulated protein78 (GRP78) protein was assessed by immunohistochemistry. Results Com⁃ pared 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.

Key words: pancreatitis, acute necrotizing, acute disease, intestinal mucosa, Emodin, apoptosis, rats, Sprague-Dawley, severe acute pancreatitis, glucose-regulated protein78