碘化N-正丁基氟哌啶醇抑制血管紧张素Ⅱ刺激血管平滑肌细胞ERK1/2和cAMP反应元件结合蛋白的表达

N-n-butyl Haloperidol Iodide Inhibits the Expression of ERK1/2 and cAMP Response Element Binding Protein Induced by Angiotensin Ⅱ in Rat Vascular Smooth Muscle Cells

目的:探讨碘化N-正丁基氟哌啶醇(F2)对血管紧张素Ⅱ(AngⅡ)刺激血管平滑肌细胞(VSMCs)ERK1/2和cAMP反应元件结合(CREB)蛋白表达的影响。方法:原代培养大鼠胸主动脉VSMCs;用Western blot法检测ERK1/2,p-ERK1/2,CREB和p-CREB蛋白表达。结果:AngⅡ可增加VSMCsp-ERK1/2和p-CREB蛋白表达,而不增加ERK1/2和CREB蛋白表达;F2(10-8,10-7和10-6mol/L)剂量-依赖地降低AngⅡ刺激的p-ERK1/2和p-CREB蛋白表达。结论:F2抑制AngⅡ刺激VSMCsERK1/2和CREB蛋白磷酸化,这可能是其抑制VSMCs增殖的机制。

Objective： To investigate the inhibitory effects N-n-butyl halopeddol iodide（F2）on expression of ERK1/2 and cAMP response element binding （CREB）protein induced by angiotensin Ⅱ in rat vascular smooth muscle cells （VSMC3）. Methods： The primary rat thoracic aortic VSMCs were cultured in vitro. The levels of ERK1/2, p-ERK1/2, CREB and p-CREB were assessed by Western blot. Results： Ang II increased the expression of p-ERK1/2 and p-CREB but not ERK1/2 and CREB protein. F2 （10^-8, 10^-7 and 10^-6mol/L）concentration-dependenfly decreased the expression of p-ERK1/2 and p-CREB. Conclusion： F2 inhibits the phosphorylation of ERK1/2 and CREB protein, which may be the mechanisms of its inhibitory effects on the proliferation of VSMCs.