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)E-cadherin,α-SMA表达的影响。方法体外培养NRK52E细胞,经Ang-(1-7)和AngⅡ(终浓度均为10^(-6)mol/L)干预24、48、72、96 h后,应用细胞免疫化学法检测E-cadherin、α-SMA蛋白的表达;采用实时荧光定量PCR(RTPCR)检测细胞中E-cadherin和α-SMA mRNA表达水平的变化。结果 AngⅡ作用96 h后,E-cadherin蛋白及E-cadherinmRNA表达显著减弱(P<0.05),α-SMA蛋白及α-SMA 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E-cadherin mRNA的表达增强(P<0.05),α-SMA蛋白及α-SMA mRNA表达减弱(P<0.05)。结论 Ang-(1-7)能够抑制AngⅡ诱导的α-SMA的表达,上调E-cadherin的表达。
Objective To investigate the influence of angiotensin-（1-7）[Ang-（l-7）]on expression of E-cadherin and a-SMA induced by angiotensionⅡ（AngⅡ） in rat＇s tubular epithelial cells.Methods The NRK52E were maintained and sub cultured,and then treated with Ang-（1-7）（10^（-6）mol/L） and AngⅡ（10^（-6）mol/L） for 24,48,72,96 hours,the protein expressions of E-cadherin andα-SMA were detect by immunocytochemistry method;The mRNA expression of E-cadherin and a-SMA was detected by real time PCR（RT-PCR）.Results Treated with angⅡafter 96 h,the protein and mRNA expression of E-cadherin decreased significantly（P0.05 ）,but the protein and mRNA expression ofα-SMA increased significantly （P0.05）;treated with AngⅡand Ang-（1-7）,the protein and mRNA expression of E-cadherin increased significantly （P0.05）,but the protein and mRNA expression ofα-SMA decreased significantly（P0.05）.Conclusion Ang-（1-7） can inhibit the expression ofα-SMA induced by AngⅡand up regulate the expression of E-cadherin.
出处
《疑难病杂志》
CAS
2011年第5期366-368,F0003,共4页
Chinese Journal of Difficult and Complicated Cases
基金
国家自然科学基金(No.30771008)
