碘化N-正丁基氟哌啶醇对缺氧血管平滑肌细胞增殖的影响及其作用机制的研究

目的:研究碘化N-正丁基氟哌啶醇(F2)对缺氧大鼠胸主动脉平滑肌细胞(SMCs)增殖的影响,并探讨其作用机制是否与早期生长反应基因-1(egr-1)有关。方法:取第3~4代培养的大鼠胸主动脉SMCs制作缺氧模型,应用噻唑蓝比色法检测细胞增殖情况,流式细胞术测定细胞周期,蛋白印迹杂交方法检测Egr-1及血小板源生长因子(PDGF-A)蛋白表达情况。结果:与缺氧组比,反义寡核苷酸组及F2组比色吸光度A值、细胞周期S G2/M期比例均下降(P<0.01),Egr-1及PDGF-A蛋白表达均减少。结论:F2可通过抑制Egr-1蛋白表达来抑制缺氧SMCs的过度增殖。

Effect and Mechanism of N-n-butyl Haloperidol Iodide on Hypoxia-induced Proliferation of Vascular Smooth Muscle Cells in vitro

Objective : To investigate the effect and mechanism of N-n-butyl haloperidol iodide(F2)on hypoxia-induced proliferation of rat thoracic aortic smooth muscle cells(SMCs)in vitro,and to indicate the relationship between the effect of F2 and the express of early growth response gene-1(egr-1).Methods: Passages 3 to 4 of cultured rat thoracic aortic SMCs were used to establish hypoxia models.The viability of VSMC was detected by mono-nuclear cell direct cytotoxicity assay.The cell cycle was analyzed by flow cytometry.The levels of Egr-1 and PDGF-A were assessed by Western blot.Results: Compared with the hypoxia group,the absorption value,proliferation index and the levels of Egr-1 and PDGFA of antisense oligodeoxynucleotide group and F2 group were all decreased.Conclusion: The inhibition of F2 on hypoxia-induced proliferation of rat thoracic aortic SMCs in vitro is mediated by Egr-1.