内质网应激及内质网应激诱导的细胞凋亡在糖尿病大鼠的胃平滑肌细胞中被激活。
ER stress and ER stress-induced apoptosis are activated in gastric SMCs in diabetic rats.
作者信息
Chen Xia, Fu Xiang-Sheng, Li Chang-Ping, Zhao Hong-Xian
机构信息
Xia Chen, Xiang-Sheng Fu, Chang-Ping Li, Department of Gastroenterology, Affiliated Hospital of Luzhou Medical College, Luzhou 646000, Sichuan Province, China.
出版信息
World J Gastroenterol. 2014 Jul 7;20(25):8260-7. doi: 10.3748/wjg.v20.i25.8260.
AIM
To investigate the gastric muscle injury caused by endoplasmic reticulum (ER) stress in rats with diabetic gastroparesis.
METHODS
Forty rats were randomly divided into two groups: a control group and a diabetic group. Diabetes was induced by intraperitoneal injection of 60 mg/kg of streptozotocin. Gastric emptying was determined at the 4(th) and 12(th) week. The ultrastructural changes in gastric smooth muscle cells (SMCs) were investigated by transmission electron microscopy. TdT-mediated dUTP nick end labeling (TUNEL) assay was performed to assess apoptosis of SMCs. Expression of the ER stress marker, glucose-regulated protein 78 (GRP78), and the ER-specific apoptosis mediator, caspase-12 protein, was determined by immunohistochemistry.
RESULTS
Gastric emptying was significantly lower in the diabetic rats than in the control rats at the 12(th) wk (40.71% ± 2.50%, control rats vs 54.65% ± 5.22%, diabetic rats; P < 0.05). Swollen and distended ER with an irregular shape was observed in gastric SMCs in diabetic rats. Apoptosis of gastric SMCs increased in the diabetic rats in addition to increased expression of GRP78 and caspase-12 proteins.
CONCLUSION
ER stress and ER stress-mediated apoptosis are activated in gastric SMCs in diabetic rats with gastroparesis.
目的
研究内质网（ER）应激对糖尿病胃轻瘫大鼠胃肌损伤的影响。
方法
40只大鼠随机分为两组：对照组和糖尿病组。腹腔注射60mg/kg链脲佐菌素诱导糖尿病。分别于第4周和第12周测定胃排空情况。采用透射电镜观察胃平滑肌细胞（SMC）的超微结构变化。采用TdT介导的dUTP缺口末端标记（TUNEL）法检测SMC的凋亡情况。通过免疫组化法检测ER应激标志物葡萄糖调节蛋白78（GRP78）和ER特异性凋亡介质半胱天冬酶-12蛋白的表达。
结果
第12周时，糖尿病大鼠的胃排空明显低于对照组（对照组为54.65%±5.22%，糖尿病大鼠为40.71%±2.50%；P<0.05）。糖尿病大鼠胃SMC中可见内质网肿胀、扩张，形态不规则。糖尿病大鼠胃SMC凋亡增加，同时GRP78和半胱天冬酶-12蛋白表达增加。
结论
糖尿病胃轻瘫大鼠胃SMC中ER应激及ER应激介导的凋亡被激活。
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