血管紧张素Ⅱ对肾小球内皮细胞骨架和单层通透性的影响

目的观察血管紧张素Ⅱ(AngⅡ)对培养肾小球内皮细胞(GENC)形态、单层通透性、肌动蛋白骨架的影响,探讨AngⅡ对GENC炎性损伤的机制。方法倒置显微镜观察AngⅡ对体外培养大鼠GENC的形态影响;用二室弥散系统检测AngⅡ对GENC单层通透性的影响;用免疫细胞化学的方法观察AngⅡ对GENCF-肌动蛋白(F-actin)分布的影响。结果AngⅡ浓度大于0.1mg·L-1作用48h内观察到细胞脱落和破裂。10mg·L-1AngⅡ6、12h可使GENC单层通透性增高、F-actin解聚。结论AngⅡ引起GENC脱落和破裂呈时间和剂量依赖性;AngⅡ引起内皮单层通透性的增高的机制可能与F-actin解聚相关;

Effects of F-actin and monolayer permeability on the injury of rat glomerular endothelial cells induced by Angiotensin Ⅱ

Aim To investigate the mechanism of Angiotensin Ⅱ (AngⅡ) induced injury on the culturedrat glomerular endothelial cell(GENC) .Methods GENC was isolated and cultured from Wistar rat in vitro,the effects of AngⅡ on morphology,monolayer permeability,F-actin of GENC were observed,F-actin expression was evaluated by immunocytochemistry.Permeability was assessed as diffusion of bovine serum albumin/(biotin-BSA) across the monolayer,The biotin-BSA concentrations were measured by capture enzyme-linkd immunosorbent assay.Results AngⅡ in the concentration larger than 0.1 mg·L-1 induced detachment and rupture of GENC within 48 h.10 mg·L-1 of AngⅡinduced the increased permeability of GENC monolayer, depolymerization of F-actin within 12 h.Conclusions 1 The detachment and rupture of GENC induced by AngⅡ depends on the exposed concentration and time.2 The increased permeability of GENC monolayer induced by AngⅡ is correlated with the depolymerization of F-actin.