摘要
目的探讨糖尿病大鼠胃平滑肌细胞凋亡机制及大黄素干预机制。方法 SD大鼠随机分为对照组、糖尿病组及大黄素组。造模10周时检测胃排空;脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(TUNEL)检测胃平滑肌细胞凋亡;免疫组织化学检测胃平滑肌细胞葡萄糖调节蛋白78(GRP78)、Caspase-12蛋白表达。结果 1与对照组比较,糖尿病组大鼠胃内色素残留率显著增高(P<0.05);与糖尿病组比较,大黄素组胃内色素残留率显著下降(P<0.05)。2糖尿病组大鼠较对照组的胃平滑肌细胞凋亡、GRP78及Caspase-12蛋白表达显著增高(P<0.05);与糖尿病组比较,大黄素组大鼠胃平滑肌细胞凋亡、GRP78及Caspase-12蛋白表达显著降低。结论内质网应激(ERS)途径可能介导糖尿病大鼠胃平滑肌细胞凋亡。大黄素可能通过减少ERS介导的胃平滑肌细胞凋亡,改善糖尿病大鼠胃排空功能。
【Objective】 To investigate the mechanism of apoptosis of gastric smooth muscle cells(SMCs)in diabetic rats, and the mechanism involving the effect of Emodin on SMCs in diabetic rats. 【Methods】 SD rats were randomly divided into control group, diabetic group and Emodin group. Gastric emptying was determined in the 10 th week. Apoptosis of gastric SMCs was detected by TUNEL method. Expressions of glucoseregulated protein 78(GRP78) and Caspase-12 protein were detected by immunohistochemistry. 【Results】 1The rate of gastric residual pigment was significantly increased in the diabetic group than in the control rats(P〈0.05). Compared with the diabetic group, the rate of gastric residual pigment was significantly decreased in the Emodin group(P〈0.05). 2 The cell apoptosis and the expressions of GRP78 and Caspase-12 protein in gastric smooth muscle cells were obviously increased in the diabetic group than in the control group(P〈0.05). Compared with the diabetic group, the cell apoptosis and the expressions of GRP78 and Caspase-12 protein in gastric smooth muscle cells were declined obviously in the Emodin group(P〈0.05). 【Conclusions】Emodin can improve the gastric emptying, which may be involved with the reduction of apoptosis of gastric SMCs in diabetic rats induced by endoplasmic reticulum(ER) stress pathway.
出处
《中国现代医学杂志》
CAS
北大核心
2015年第27期18-21,共4页
China Journal of Modern Medicine
基金
四川省泸州市科技局重点项目[No:2009-S-15(5/7)]
四川省卫生厅资助项目(No:100242)
关键词
大黄素
糖尿病胃轻瘫
胃平滑肌
凋亡
内质网应激
Emodin
gastroparesis
gastric smooth muscle
apoptosis
endoplasmic reticulum stress