摘要
目的在人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs)水平以及大鼠体内实验中,探讨抵抗素(resistin)能否通过内质网(ER)应激导致血管内皮细胞产生胰岛素抵抗(IR)。方法培养HUVECs(control组)并应用抵抗素(R组)或内质网应激缓解剂牛磺熊去氧胆酸(tudca组)处理细胞,以胰岛素处理(Ⅰ组)为阳性对照组,Western印迹检测ER应激标志蛋白GRP78、P-akt和P-e NOS的相对表达量;将15只大鼠随机分为control、R和tudca 3组,制备各组大鼠胸主动脉血管环,检测胰岛素诱导的血管舒张能力,并行HE染色观察血管的形态学改变。结果 Western印迹检测结果显示,与其余3组比较,R组GRP78蛋白表达量显著增高(P<0.01),与Ⅰ组比较P-akt和P-e NOS蛋白表达量明显降低(P<0.01)。R组血管对胰岛素诱导的舒张作用明显减弱,与control组相比差异有统计学意义(P<0.01)。HE染色显示,R组大鼠血管壁明显增厚,平滑肌显著增生。结论抵抗素能通过ER应激途径致血管内皮细胞产生IR。
Objective To identify the role of resistin in insulin resistance（IR） by endoplasmic reticulum （ER） stress in human umbilical vein endothelial cells （HUVECs） and in rats. Methods HUVECs were cultured in vitro and disposed by resistin （R） or tauro ursodesoxycholic acid （tudca）. Expressions of GRP78, P-akt and P-eNOS were determined using Western blotting. Thoracic aortic rings were made and their dilation function exposed to different concentrations of insulin was detected. Changes of vascular morphology were observed by HE staining. Results Results of Western blotting showed that expression of GRP78 was remarkably increased, hut P-akt and P-eNOS were markedly decreased in R group. However, there was no difference in expressions of GRP78, P-akt and P-eNOS between tudca group and control group. The insulin induced vasodilation was decreased in R group and there was no difference between tudca group and control. Using HE staining, the R group showed significant medial thickening and proliferation of smooth muscle. Conclusion Resistin can induce insulin resistance in vascular endothelium cells by ER stress.
出处
《军事医学》
CAS
CSCD
北大核心
2015年第8期607-609,625,共4页
Military Medical Sciences
关键词
抵抗素
内质网应激
胰岛素抵抗
内皮细胞
resistin
endoplasmic reticulum stress
insulin resisitance
endothelial cells
