氟伐他汀抑制高血压大鼠血管平滑肌细胞增殖

目的:探讨氟伐他汀对自发性高血压大鼠血管平滑肌细胞增殖的抑制作用。方法:培养自发性高血压大鼠主动脉血管平滑肌细胞,不同浓度血管紧张素Ⅱ(AngⅡ)、血小板源生长因子(PDGF)、氟伐他汀及甲羟戊酸干预后,行细胞计数和³H]-TdR掺入率测定。结果:①氟伐他汀呈浓度依赖性抑制10^-6mol/LAngⅡ和10μg/LPDGF刺激诱导的血管平滑肌细胞数和³H]-TdR掺入率增加;②10^-3mol/L甲羟戊酸几乎完全逆转氟伐他汀对血管平滑肌细胞增殖的抑制作用。结论:氟伐他汀抑制AngⅡ和PDGF诱导的高血压大鼠血管平滑肌细胞增殖;甲羟戊酸代谢途径可能参与血管平滑肌细胞增殖过程。

Inhibitory effect of fluvastatin on the proliferation of vascular smooth muscle cells in spontaneously hypertensive rats

AIM:To investigate the effect of fluvastatin on the proliferation of vascular smooth muscle cells derived from spontaneously hypertensive rats. METHODS:The aorta smooth muscle cells(ASMCs)of spontaneously hypertensive rats were cultured,and proliferation of cells were detected by measuring cell number and ³H]-thymidine(³H]-TdR)incorporation after incubation with AngⅡ,PDGF,fluvastatin and mevalonate acid.RESULTS:(1) The increased cell number and ³H]-TdR incorporation stimulated with AngII(10^-6 mol/L) and PDGF(10 μg/L) were significantly inhibited by fluvastatin in a concentration-dependent manner (10^-5-10^-7mol/L); (2) The inhibitory effect of fluvastatin was almost completely reversed by mevalonate acid(10^-3 mol/L).CONCLUSION:The proliferation of ASMCs induced by Ang Ⅱ and PDGF was inhibited by fluvastatin, suggesting that mevalonate acid pathway may play an important role in the proliferation of ASMCs.