摘要
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 [3 H]-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 10 μg/LPDGF刺激诱导的血管平滑肌细胞数和 [3 H]-TdR掺入率增加 ;② 10 -3 mol/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。
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 -thymidine(-TdR) incorporation after incubation with Ang Ⅱ, PDGF, fluvastatin and mevalonate acid. RESULTS: (1) The increased cell number and -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 -7 mol/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.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2002年第5期483-485,共3页
Chinese Journal of Pathophysiology
基金
福建省自然科学基金资助项目 (C9910 0 0 7)
高等学校骨干教师资助项目 (0 0A0 0 4 )
