【摘要】 目的探讨血管紧张素-(1-7)[Ang-(1-7)]对血管紧张素Ⅱ(AngⅡ)诱导的大鼠肾小管上皮细胞(NRK52E)表型转化及ERK1/2信号分子在转分化过程中的作用。方法体外培养NRK52E,经Ang-(1-7)和AngⅡ(终浓度均为10-6mol/L)干预24、48、72、96 h后,应用细胞免疫化学法检测E-cadherin、α-SMA的表达;干预72、96 h后,应用Western blot法检测P-ERK1/2表达水平的变化。结果 AngⅡ作用96 h后,E-cadherin的表达显著减弱(P<0.05),α-SMA的表达显著增强(P<0.05),P-ERK1/2表达显著增强(P<0.05);同时加入Ang-(1-7)后,与AngⅡ组比较,E-cadherin的表达显著增强(P<0.05),α-SMA的表达显著减弱(P<0.05),P-ERK1/2表达显著减弱(P<0.05)。结论 Ang-(1-7)能够抑制AngⅡ诱导的大鼠NRK52E表型转化,ERK1/2信号通路参与了肾小管上皮细胞转分化过程。更多还原

【Abstract】 Objective To explore the role of ERK1/2 signaling pathway on angiotensin-(1-7) inhibit rat′s tubular epithelial myofibroblast transdifferentiation induced by angiotensinⅡ.Methods NRK52E were maintained and sub-cultured.The NRK52E cells were stimulated by angiotensin-(1-7) and angiotensinⅡ(both 10-6 mol/L),cultured for 24,48,72,96 h,we detected the expressions of E-cadherin and α-SMA by immunocytochemistry method;cultured for 72,96 h,ERK1/2,detected by Western blot.Results The cells,cultured for 96h,expressions of α-SMA and P-ERK1/2 of AngⅡ group increased significantly than that of control group(P<0.05),expressions of E-cadherin of AngⅡ group decreased significantly than that of control group(P<0.05);expressions of α-SMA and P-ERK1/2 of AngⅡ+Ang-(1-7) group decreased significantly than that of AngⅡ group at the same time(P<0.05),expressions of E-cadherin of AngⅡ+Ang-(1-7) group increased than that of AngⅡ group at the same time(P<0.05).Conclusion Ang-(1-7) can inhibit AngⅡ-induced tubular epithelial myofibroblast transdifferentiation.ERK1/2 signaling pathway plays an important role in rat′s tubular epithelial myofibroblast transdifferentiation.更多还原