中文摘要：

目的探讨大黄素对糖尿病大鼠肠平滑肌细胞凋亡机制及调控机制。方法SD大鼠分为对照组、糖尿病组与大黄素组，成模10周时，检测小肠推进率；TUNEL法测肠平滑肌细胞凋亡；免疫组织化学测细胞葡萄糖调节蛋白78（GRP78）及Caspase-12蛋白表这。结果糖尿病组与大黄素组大鼠于成模后出现多尿、多饮、多食、体质量减轻症状；血糖水平显著增高（P〈0．05）。成模10周时，与对照组比较，糖尿病组大鼠小肠推进率显著下降（P〈0．05），肠平滑肌细胞凋亡率、GRP78、Caspase-12蛋白表达显著增加（P〈0．05）。与糖尿病组比较，大黄素组小肠推进率显著增高（P〈0．05），肠平滑肌细胞凋亡率、GRP78、Caspase-12蛋白表达显著降低（P〈0．05）。结论内质网应激途径介导了糖尿病大鼠肠平滑肌细胞凋亡；大黄素可能降低糖尿病大鼠肠平滑肌内质网应激介导的细胞凋亡，从而改善肠动力。

英文摘要：

Objective To investigate the regulation of emodin on endoplasmic reticulum stress response of intestinal smooth muscle in diabetic rats. Methods SD rats were divided into control group,diabetic group and emodin group randomly. 10 weeks lat- er, the intestinal motility,apoptosis, GRP78 and Caspase-12 proteins of intestinal smooth muscle cell were detected through intesti- nal propulsion rate, TUNEL and immunohistochemistry respectively. Results The rats in diabetic group and emodin group ap- peared the symptoms of diabetes. 10 weeks later, compared with control group, the intestinal propulsion rate of the diabetic group decreased significantly （P〈0.05）, cell apoptotic rate, GRP78 and Caspase-12 proteins of intestinal smooth muscle increased signifi- cantly（P〈0.05）. Compared with diabetic group,the intestinal propulsion rate of emodin group increased significantly （P〈0.05）, cell apoptotic rate,GRP78 and Caspase-12 proteins of intestinal smooth muscle decreased significantly（P〈0.05）. Conclusion The endoplasmic reticulum stress may be involved in the cell apoptosis of intestinal smooth muscle in diabetic rats,which played a partial role in the pathogenesis of intestinal dynamic obstacles of diabetes. Emodin may reduce the apoptosis induced by endoplasmic reticu- lum stress of the intestinal smooth muscle in diabetic rats so as to improve the intestinal motivation.