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作 者:谢登荣 郑春华[2] 刘仁水[1] 杨全坤 罗正平[1]
机构地区:[1]湖南省怀化市第二人民医院心内科,怀化418000 [2]南昌市第一医院心内二科,南昌330008
出 处:《世界临床药物》2009年第8期474-479,共6页World Clinical Drug
摘 要:目的观察阿托伐他汀联用依帕司他对血管平滑肌细胞(VSMC)及醛糖还原酶(AR)和核因子(NF)-κB的影响,探讨阿托伐他汀联合依帕司他抗细胞增生的可能机制。方法采用高浓度葡萄糖诱导大鼠VSMC的AR基因表达,以高、中、低各浓度阿托伐他汀和依帕司他干预,培养3d,行细胞计数。并采用RT-PCR、免疫组化及原位杂交等方法,观察阿托伐他汀加依帕司他对NF-κB和AR基因表达及VSMC增生的影响。结果高浓度葡萄糖诱导时,NF-κB表达强阳性,以不同浓度阿托伐他汀和依帕司他干预,NF-κB表达逐渐减弱,10μmol/L阿托伐他汀和依帕司他组,VSMC计数显著减少。结论阿托伐他汀联合依帕司他可抑制VSMC增生及AR和NF-κB表达,且具有浓度依赖性,推测其可能通过抑制AR及NF-κB的表达从而抑制VSMC增生。Objective To observe the effect of atorvastatin and epalrestat on vascular smooth muscle cell (VSMC), aldose reductase (AR) and nucleus factor (NF)-κB, discuss the possible mechanism of resisting VSMC proliferation. Methods With the inducement of high concentration of glucose (22.5 mmol/L), AR expression was increased in the rat VSMC. Then different concentration of atorvastatin and epalrestat was added. After three day's cultivation, the cells were counted. RT-PCR, immunohistochemical methods and in situ hybridization were used to examine AR expression and VSMC proliferation. Results With the increase of the concentration of atorvastatin and epalrestat, the number of VSMC was decreased gradually. NF-κB was expressed highly at high concentration of glucose, when added with different concentration of atorvastatin and epalrestat, its expression was decreased. Conclusion atorvastatin and epalrestat could inhibit proliferation of VSMC, expression of AR and NF-κB, and showed dose-dependent. Atorvastatin and epalrestat might inhibit VSMC proliferation through inhibiting AR and NF-κB expression.
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