中国药理学通报2012，Vol.28Issue(8)：1115-1119,5.DOI:10.3969/j.issn.1001-1978.2012.08.018
碘化N-正丁基氟哌啶醇抑制机械损伤诱导的血管平滑肌细胞增殖的作用及机制
Effect and mechanism of N-n-butyl haloperidol iodide on the proliferation of rat vascular smooth muscle cells induced by mechanical injury
摘要
Abstract
Aim To investigate the inhibitory effects and mechanisms of N-n-butyl haloperidol iodide ( F2) on rat vascular smooth muscle cells (VSMCs) proliferation induced by mechanical injury in vitro. Methods The primarily cultured rat thoracic aortic SMCs were used to establish mechanical injury models in vitro. The proliferation activity of VSMCs was analyzed by cell counting Kit-8 ( CCK-8) assay. And the cell cycle was analyzed by flow cytometry. The levels of Egr-1 and p-ERK, p-MEK were assessed by Western blot. The expressions of MEK and Egr-1 mRNA were tested by real time RT-PCR. Results F2 concentration-de-pendently inhibited VSMCs proliferation, decreased the cell survival rate and DNA synthesis in VSMCs stimu- lated by mechanical injury, which led to the increase of cell numbers of G0/G1 phase and a reduction in those of G2/M phase, and restrained the activation of MEK/ERK by attenuating phospho-MEK/ERK and Egr-1 proteins expression as well as down-regulated the overexpression of MEK and Egr-1 after mechanical injury. Conclusion F2 obviously inhibits vascular smooth muscle cell proliferation after mechanical injury in vitro, and its mechanisms may be involved in inhibiting the MEK/ERK/Egr-1 signaling pathway.关键词
碘化N-正丁基氟哌啶醇/机械损伤/血管平滑肌细胞/增殖/丝裂原活化蛋白激酶/早期生长反应基因-1Key words
N-n-butyl haloperidol iodide/ mechanical injury/ vascular smooth muscle cells/ proliferation/ mitogen-activated protein kinase/ early growth response gene-1引用本文复制引用
黄展勤,韩莎莎,李金玉,郑燕珊,刘幸平,高分飞,张艳美,石刚刚..碘化N-正丁基氟哌啶醇抑制机械损伤诱导的血管平滑肌细胞增殖的作用及机制[J].中国药理学通报,2012,28(8):1115-1119,5.基金项目
国家自然科学基金资助项目(No 30901810) （No 30901810）
广东省自然科学基金资助项目(No 9151063201000072)广东省医学科研基金(No B2007120) （No 9151063201000072）
