血管紧张素-(1-7)对血管紧张素Ⅱ诱导的大鼠肾小管上皮细胞转分化的影响  

Influence of angiotensin-(1-7) on angiotensinⅡ induced rat's tubular epithelial-myofibroblast transdifferentiation

作　　者：袁波[1] 贺红焰[2] 王明勇[3] 刘建[1] 

机构地区：[1]泸州医学院附属医院肾病内科,四川泸州646000 [2]泸州医学院附属医院病理科,四川泸州646000 [3]泸州医学院附属医院医学实验中心,四川泸州646000

出　　处：《细胞与分子免疫学杂志》2011年第9期962-964,968,共4页Chinese Journal of Cellular and Molecular Immunology

基　　金：国家自然科学基金资助项目(30771008)

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)表型转化及细胞外基质分泌的影响。方法:体外培养NRK52E细胞,经Ang-(1-7)和AngⅡ(终浓度均为1×10-6mol/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;应用ELISA法检测细胞上清液中Ⅰ型胶原(ColⅠ)和纤维黏连蛋白(FN)的表达;采用实时荧光定量PCR(Real-tim e PCR)检测细胞中E-cadherin、α-SMA、ColⅠ和FN mRNA表达水平的变化。结果:AngⅡ作用96 h后,E-cadherin蛋白及mRNA表达显著减弱(P<0.05),α-SMA、ColⅠ、FN蛋白及mRNA表达显著增强(P<0.05);同时加入Ang-(1-7)后,与AngⅡ组比较,E-cadherin蛋白及mRNA的表达增强(P<0.05),α-SMA、ColⅠ、FN蛋白及mRNA表达减弱(P<0.05)。结论:Ang-(1-7)能够抑制AngⅡ诱导的大鼠肾小管上皮细胞表型转化及细胞外基质的分泌。AIM： To explore the influence of angiotensin-（1-7）[Ang-（1-7）] on angiotensionⅡ（AngⅡ） induced rat＇s tubular epithelial-myofibroblast transdifferentiation and the secretion of extracellular matrix.METHODS： The NRK52E were maintained and sub-cultured treated with Ang-（1-7）（10-6 mmol/L） and AngⅡ（10-6 mmol/L） for 24,48,72,96 hours,we detect the protein expressions of E-cadherin andα-SMA by immunocytochemistry method;The content of ColⅠand FN in the cultured supernatant were measured by ELISA;The mRNA expression of E-cadherin,α-SMA,ColⅠand FN was detected by real-time PCR.RESULTS： Treat with angⅡ 96 h,the protein and mRNA expression of E-cadherin decreased significantly（P0.05）,but the protein and mRNA expressionα-SMA,colⅠand FN increased significantly（P0.05）;treat with AngⅡand Ang-（1-7）,the protein and mRNA expression of E-cadherin increased significantly（P0.05）,but the protein and mRNA expressionα-SMA,colⅠand FN decreased significantly（P0.05）.CONCLUSION： Ang-（1-7） can inhibits AngⅡ-induced rat＇s tubular epithelial myofibroblast transdifferentiation and decrease the secretion of FN and ColⅠ.

关 键 词：血管紧张素-(1-7) 血管紧张素Ⅱ 肾小管上皮细胞转分化 

分 类 号：R363.1[医药卫生—病理学] R363.2[医药卫生—基础医学]