【摘要】 目的探讨瞬时受体电位阳离子通道6(TRPC6)在血管紧张素Ⅱ(AngⅡ)诱导大鼠的血管平滑肌细胞(VSMC)增殖中的作用。方法应用组织贴块法培养大鼠主动脉VSMC,用AngⅡ刺激VSMC建立细胞增殖模型,应用Western blot技术检测平滑肌细胞的TRPC6表达水平,采用四甲基偶氮唑蓝比色法(MTT法)检测不同浓度的SKF96365(TRPC通道阻断剂)和不同浓度的flufenamicacid(TRPC6激动剂)对VSMC增殖的影响。结果Western blot显示在VSMC中TRPC6通道蛋白表达水平很高。用SKF96365(10、50、100μmol/L)阻断TRPC6通道后,经过72h的作用抑制AngⅡ诱导的VSMC的增殖,且呈剂量依赖性。用flufenamicacid(10、20、40μmol/L)激动TRPC6通道,经过24h的作用促进了VSMC的增殖。结论在AngⅡ诱导大鼠的血管平滑肌细胞增殖中,TRPC6通道起着很重要的作用。更多还原

【Abstract】 Objective To investigate the effect of transient receptor potential cation channel 6 (TRPC 6)on angiotensin Ⅱ(AngⅡ)induced vascular smooth muscle cells(VSMC)proliferation.Methods VSMCs were cultured by tissue explant method.Cell proliferation model was established by stimulation with AngII.Western blot was detected the expression of transient receptor potential C (TRPC) channels in VSMC.Cell proliferation was measured by MTT assay to evaluate the effects of SKF96365 (TRPC antagonist) and flufenamic acid (TRPC6 agonist) in different concetration on Ang Ⅱ-induced VSMC proliferation.Results The expression of TRPC6 channel was high in VSMC.After exposured to SKF96365(10,50,100 μmol/L)for 72h,the growth of VSMC was inhibited dose-dependently.The VSMC proliferation could be induced by flufenamic acid (10,20,40 μmol/L)dose-dependently which could be activated by TRPC6 channel.Conclusion TRPC6 channel have a Critical role in the proliferation of angiotensin Ⅱ-induced vascular smooth muscle cell.更多还原