血管紧张素转换酶2基因转染抑制平滑肌细胞增殖

Effect of ACE2 gene transfection on the proliferation of vascular smooth muscle cells in rats

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.