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目的探讨碘化N-正丁基氟哌啶醇(F2)对机械损伤所致血管平滑肌细胞(VSMCs)增殖的抑制作用及其机制。方法原代培养大鼠胸主动脉VSMCs,体外建立机械划伤致VSMCs增殖模型,采用Cell Counting Kit-8(CCK-8)法检测细胞增殖情况;流式细胞术法测定细胞周期;Western blot法检测p-MEK,p-ERK,Egr-1蛋白表达;Real Time RT-PCR检测MEK和Egr-1 mRNA表达。结果 F2剂量依赖地抑制机械损伤所致VSMCs增殖,降低损伤刺激下VSMCs的生存率和DNA合成,使G0/G1期细胞比例升高,G2/M期细胞百分比下降,并且抑制损伤后VSMCs中MEK/ERK的活化,使p-MEK/ERK蛋白表达降低,同时下调损伤后MEK和Egr-1的高表达。结论 F2对机械损伤所致血管平滑肌细胞增殖有明显抑制作用,其机制可能与影响MEK/ERK/Egr-1信号途径有关。
Objective To investigate the inhibitory effect of n-butyl haloperidol iodide (F2) on the proliferation of vascular smooth muscle cells (VSMCs) induced by mechanical injury and its mechanism. Methods VSMCs were primarily cultured in rat thoracic aorta and proliferation of VSMCs induced by mechanical injury was established in vitro. Cell proliferation was detected by Cell Counting Kit-8 (CCK-8), cell cycle was determined by flow cytometry, Western blot The expressions of p-MEK, p-ERK and Egr-1 were detected by real-time RT-PCR. The mRNA expressions of MEK and Egr-1 were detected by Real Time RT-PCR. Results F2 dose-dependently inhibited the proliferation of VSMCs induced by mechanical injury and decreased the survival rate and DNA synthesis of VSMCs under stimulation. The proportion of cells in G0 / G1 phase increased and the percentage of cells in G2 / M phase decreased, and inhibited the expression of MEK / ERK activation, so that p-MEK / ERK protein expression decreased, while down-regulation MEK and Egr-1 high expression. Conclusion The inhibitory effect of F2 on proliferation of vascular smooth muscle cells induced by mechanical injury may be related to the mechanism of MEK / ERK / Egr-1 signaling pathway.