军事医学
軍事醫學
군사의학
BULLETIN OF THE ACADEMY OF MILITARY MEDICAL SCIENCES
2015年
8期
607-609,625
,共4页
抵抗素%内质网应激%胰岛素抵抗%内皮细胞
牴抗素%內質網應激%胰島素牴抗%內皮細胞
저항소%내질망응격%이도소저항%내피세포
resistin%endoplasmic reticulum stress%insulin resisitance%endothelial cells
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－eNOS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－eNOS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。
目的：在人臍靜脈內皮細胞（ human umbilical vein endothelial cells，HUVECs）水平以及大鼠體內實驗中，探討牴抗素（resistin）能否通過內質網（ER）應激導緻血管內皮細胞產生胰島素牴抗（IR）。方法培養HUVECs （ control組）併應用牴抗素（ R組）或內質網應激緩解劑牛磺熊去氧膽痠（ tudca組）處理細胞，以胰島素處理（Ⅰ組）為暘性對照組，Western印跡檢測ER應激標誌蛋白GRP78、P－akt和P－eNOS的相對錶達量；將15隻大鼠隨機分為control、R和tudca 3組，製備各組大鼠胸主動脈血管環，檢測胰島素誘導的血管舒張能力，併行HE染色觀察血管的形態學改變。結果 Western印跡檢測結果顯示，與其餘3組比較，R組GRP78蛋白錶達量顯著增高（P＜0．01），與Ⅰ組比較P－akt和P－eNOS蛋白錶達量明顯降低（ P＜0．01）。 R組血管對胰島素誘導的舒張作用明顯減弱，與control組相比差異有統計學意義（P＜0．01）。 HE 染色顯示，R組大鼠血管壁明顯增厚，平滑肌顯著增生。結論牴抗素能通過ER應激途徑緻血管內皮細胞產生IR。
목적：재인제정맥내피세포（ human umbilical vein endothelial cells，HUVECs）수평이급대서체내실험중，탐토저항소（resistin）능부통과내질망（ER）응격도치혈관내피세포산생이도소저항（IR）。방법배양HUVECs （ control조）병응용저항소（ R조）혹내질망응격완해제우광웅거양담산（ tudca조）처리세포，이이도소처리（Ⅰ조）위양성대조조，Western인적검측ER응격표지단백GRP78、P－akt화P－eNOS적상대표체량；장15지대서수궤분위control、R화tudca 3조，제비각조대서흉주동맥혈관배，검측이도소유도적혈관서장능력，병행HE염색관찰혈관적형태학개변。결과 Western인적검측결과현시，여기여3조비교，R조GRP78단백표체량현저증고（P＜0．01），여Ⅰ조비교P－akt화P－eNOS단백표체량명현강저（ P＜0．01）。 R조혈관대이도소유도적서장작용명현감약，여control조상비차이유통계학의의（P＜0．01）。 HE 염색현시，R조대서혈관벽명현증후，평활기현저증생。결론저항소능통과ER응격도경치혈관내피세포산생IR。
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,but 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.
