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目的探讨阿托伐他汀(atorvastatin)对血管紧张素Ⅱ(AngⅡ)诱导的心房肌细胞结缔组织生长因子(con-nective tissue growth factor,CTGF)及缝隙连接蛋白43(Connexin 43,Cx43)表达的影响。方法 18只雌雄对半1周龄左右Wistar大鼠,用于体外心房肌细胞的分离培养与鉴定。设置6组(n=18):正常对照组、AngⅡ(终浓度1μmol/L)组、AngⅡ+二甲基亚砜(DMSO)组、AngⅡ+atorvastatin(0.1、1.0、10μmol/L)组,作用72 h后RT-PCR分别检测CTGF、TGF-β1及Cx43的mRNA表达。结果与正常对照组相比,AngⅡ组CTGF、TGF-β1和Cx43 mRNA表达呈显著增加(P<0.05),阿托伐他汀逆转上述变化,10μmol/L组作用最强(P<0.05),而作为溶剂的DMSO无明显作用(P>0.05)。结论阿托伐他汀可能通过抑制AngⅡ诱导的心房肌细胞CTGF mRNA的高表达来减轻心房纤维化,同时可能通过下调Cx43 mRNA的表达来逆转缝隙连接蛋白的重构,最终减低房颤发生率。
Objective To investigate the effect of atorvastatin on the expression of connective tissue growth factor (CTGF) and connexin 43 (Cx43) in atrial myocytes induced by angiotensin Ⅱ (AngⅡ) . Methods 18 male and female Wistar rats, half and one week old, were used for isolation, culture and identification of atrial myocytes in vitro. Six groups (n = 18) were established: normal control group, Ang Ⅱ (1μmol / L), AngⅡ + DMSO group and AngⅡ + atorvastatin After 72 h, the mRNA expressions of CTGF, TGF-β1 and Cx43 were detected by RT-PCR. Results Compared with the normal control group, the expression of CTGF, TGF-β1 and Cx43 mRNA in AngⅡ group was significantly increased (P <0.05), atorvastatin reversed the above changes, the effect was the strongest in 10μmol / L group (P <0.05) DMSO as a solvent had no significant effect (P> 0.05). Conclusions Atorvastatin may ameliorate atrial fibrosis by inhibiting the high expression of CTGF mRNA induced by Ang Ⅱ, and at the same time, it may reverse the remodeling of connexin by down-regulating the expression of Cx43 mRNA and ultimately reduce the incidence of atrial fibrillation.