摘要
目的:探讨内质网应激是否参与糖尿病大鼠胃黏膜损伤以及大黄素对其调节。方法:SD大鼠随机分为对照组、糖尿病组与大黄素组,成模10周后,免疫组化法检测各组胃黏膜细胞GRP78,Caspase12蛋白表达情况。结果:①与对照组相比,糖尿病组与大黄素组大鼠于造模后均出现多尿、多饮、多食症状,成模10周时,体重减轻(P<0.05);血糖浓度显著增高(P<0.05)。②与对照组相比,糖尿病组大鼠胃黏膜GRP78、Caspase12蛋白阳性表达细胞显著增多(P<0.05);与糖尿病组相比,大黄素组GRP78、Caspase12蛋白阳性表达的胃黏膜细胞显著减少(P<0.05)。结论:内质网应激途径可能介导了糖尿病大鼠胃黏膜损伤,大黄素可降低糖尿病大鼠胃黏膜细胞的内质网应激反应,从而实现对胃黏膜的修复。
Objective： To investigate the regulation of emodin on endoplasmic reticulum stress of gastric mucosa in diabetic rats. Methods： SD rats were randomly divided into control group, diabetic group and emodin group. Ten weeks after the diabetic model was established and the glucose-regulated protein 78 （GRP78） and Caspasel2 were detected by immunohistochemistry. Results： （1） Compared with control group, typical symptoms of diabetes mellitus appeared in diabetic group and emodin group. （2） Compared with control group, the GRP78 and Caspase12 were significantly higher in diabetic group （P 〈 0.05）. Compared with diabetic group, the GRP78 and Caspase12 were significantly lower in emodin group （P 〈 0.05）. Conclusion： Endoplasmic reticulum stress may induce the injury of gastric mucosa of diabetic rats. Emodin can decrease endoplasmic reticulum stress of gastric mucosa so as to reduce its injury.
出处
《泸州医学院学报》
2014年第3期239-242,共4页
Journal of Luzhou Medical College
基金
四川省卫生厅资助项目(100242)
泸州市科技局重点项目(2009-S-151517)
关键词
大黄素
糖尿病
胃黏膜
凋亡
内质网应激
Emodin
Diabetes
Gastric mucosa
Apoptosis
Endoplasmic reticulum stress
