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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 investigate whether resistin can induce insulin resistance in vascular endothelial cells through endoplasmic reticulum (ER) stress in human umbilical vein endothelial cells (HUVECs) and in vivo in rats ). Methods HUVECs (control group) were cultured and treated with resistin (R group) or endoplasmic reticulum stress reliever Tauroursodeoxycholic acid (Tudca group). The cells were treated with insulin (group Ⅰ) and positive control group The relative expression of ER stress marker proteins GRP78, P-akt and Pe NOS were detected by Western blotting. Fifteen rats were randomly divided into three groups: control, R and tudca, and the thoracic aortic rings were prepared. Insulin induction Vasodilatation, parallel HE staining observed vascular morphological changes. Results Western blotting showed that compared with the other three groups, the expression of GRP78 protein in R group was significantly increased (P <0.01), and the protein expression of P-akt and P-e NOS was significantly decreased compared with the other three groups (P <0.01). Compared with the control group, the vascular relaxation of rats in R group was significantly weakened (P <0.01). HE staining showed that the vascular wall of R group was significantly thicker and smooth muscle significantly proliferated. Conclusion Resistin can induce IR in vascular endothelial cells through the ER stress pathway.