摘要
目的通过血管紧张素转换酶2(ACE2)基因转染大鼠血管平滑肌细胞(VSMC),观察其对血管紧张素Ⅱ(AngⅡ)促VSMC增殖的影响。方法将大鼠VSMC分为正常细胞组、AngⅡ组、空载体+AngⅡ组及pm—ACE2+AngⅡ组,通过CCK8细胞计数试剂盒和流式细胞仪检测各组细胞周期,观察ACE2基因转染对AngⅡ促VSMC增殖效应的影响。结果与正常细胞组相比,AngII组细胞计数明显增高,pm—ACE2+AngⅡ组与AngII组相比显著降低(0.535±0.004比0.866±0.026,P〈0.05);同时,AngⅡ组在G0/G1期细胞的百分率明显降低(58.80%±2.00%,P〈0.05),S期的则显著增高(35.90%±1.00%,P〈0.05),与AngⅡ组相比,pmACE2+AngⅡ组在Go/G,期的百分率明显升高(63.90%±1.40%,P〈0.05),S期则显著降低(27.80%±0.46%,P〈0.05)。结论ACE2基因转染能抑制Ang1I的促VSMC异常增殖效应。
Objective To investigate the effect of Ang Ⅱ on the proliferation of vascular smooth muscle cell (VSMC) in rats after the transfection of ACE2 gene. Methods pm-ACE2 was transfected into the cultured VSMC by Lipofectamine 2000. The normal cell group, Ang Ⅱ group and pcDNA3.1/Hygro( + ) transfected + Ang Ⅱ group were taken as controls respectively. After the transfection of ACE2 gene, the cell proliferative effect of Ang Ⅱ on VSMC was investigated by cell counting kit-8 ( CCK8 ) and cell cycle detection by fluorescence activated cell sorter (FACS). Results The (optical density) OD value of Ang Ⅱ group was obviously higher than that of other groups. And it was obviously lower in the pm-ACE2 + Ang Ⅱ group than the Ang Ⅱ group(0. 535 ± 0. 004 vs 0. 866 ± 0. 026, P 〈 0. 05 ). Compared with other groups, the G0/Gl stage percentage of VSMC was obviously lower in the Ang Ⅱgroup ( 58. 80% ± 2. 00% , P 〈 0. 05 ) while the percentage of S stage was obviously higher ( 35.90% ±1.00%, P 〈 0. 05 ). Compared with the AngⅡ group , the G0/Gl stage percentage of VSMC was obviously higher(63.90% + 1.40% , P 〈0. 05)in the pm-ACE2 + Ang Ⅱ group while the percentage of S stage was obviously lower( 27. 80% ±0. 46% , P 〈 0. 05 ). Condusion The over-expression of ACE2 gene can inhibit the proliferation of AngⅡ -induced VSMC.
出处
《中华医学杂志》
CAS
CSCD
北大核心
2011年第2期125-128,共4页
National Medical Journal of China