期刊文献+

碘化N-正丁基氟哌啶醇抑制兔颈总动脉球囊损伤后血管内膜和平滑肌细胞增殖的作用研究 被引量:1

Effects of N-n-butyl haloperidol iodide on the proliferation of intima and vascular muscle cells of rabbit carotid artery after balloon injury
下载PDF
导出
摘要 目的:探讨碘化N-正丁基氟哌啶醇(F2)对兔颈总动脉球囊损伤后内膜及平滑肌细胞增殖的影响。方法:30只新西兰兔随机分为假手术组、模型组、F2高剂量给药组(2mg/kg)、F2中剂量给药组(1mg/kg)、F2低剂量给药组(0.5mg/kg)。模型组及F2各给药组行左侧颈总动脉球囊损伤,各组分别于术后7d取颈总动脉段,常规病理切片,HE染色,免疫组化法测定α-actin、增殖细胞核抗原(PCNA)的表达水平。结果:与假手术组比较,模型组术后7d血管内膜厚度、内膜面积、内膜厚度/中膜厚度、内膜面积/中膜面积、血管壁细胞PCNA表达显著增加(P<0.01),F2剂量依赖地降低上述指标。与假手术组比较,模型组血管壁α-actin阳性染色减少,F2各给药组可增加血管壁平滑肌细胞中α-actin阳性染色率。结论:F2能抑制兔颈总动脉机械损伤后血管内膜和平滑肌细胞的增殖。 AIM: To investigate the effects of N-n-butyl haloperidol iodide(F2) on the proliferation of intima and vascular smooth muscle cells(VSMCs) of the rabbit carotid artery after balloon injury.METHODS: 30 New Zealand rabbits were randomly divided into Sham group,Model group,F2 high-dose treatment group(2 mg/kg),F2 medium-dose treatment group(1 mg/kg),F2 low-dose treatment group(0.5 mg/kg).After 7 days,experimental segments of arteries were harversted and subsequently progressed routine pathological sections,hematoxylin-eosin staining,PCNA expression was measured by immunohistochemical staining.RESULTS:Compared with the sham group,the intimal thickness,intimal area,intimal/medial thickness and intima-to-media area ratio of the Model group significantly increase(P0.01).F2 caused a dose-dependent reduction in these indicators.F2 dose-dependently decrease the PCNA positive rate of VSMCs in the vascular wall as compared with Model group(P0.01).CONCLUSION: F2 inhibits the proliferation of intima and VSMCs of rabbit carotid artery after balloon injury.
出处 《中国临床药理学与治疗学》 CAS CSCD 2012年第10期1112-1117,共6页 Chinese Journal of Clinical Pharmacology and Therapeutics
基金 国家自然科学基金资助项目(30901810) 广东省自然科学基金资助项目(9151063201000072)
关键词 碘化N-正丁基氟哌啶醇 机械损伤 血管内膜 血管平滑肌细胞 增殖 N-n-butyl haloperidol iodide Mechanical injury Intima Vascular smooth muscle cells Proliferation
  • 相关文献

参考文献16

  • 1Togni M, Windecker S, Cocchia R, et al. Siroli mus-eluting stents associated with paradoxic coro- nary vasoconstricdon[J]. J Am Coll Cardio, 2005, 46(2): 231-236.
  • 2Pasterkamp G, de Kleijn DP, Borst C. Arterial re- modeling in theroselerosis, restenosis and after al- teration of blood flow: potential mechanisms and clinical implications[J]. Cardiovasc Res, 2000, 45 (4) : 843-852.
  • 3Muto A, Fitzgerald TN, Pimiento JM, et al Smooth muscle cell signal transduction: implica tions of vascular biology for vascular surgeons[J]. J Vasc Surg, 2007, 45 (6S): 15-24.
  • 4House SJ, Potier M, Bisaillon J, et al. The non-ex citable smooth muscle., calcium signaling and phe notypic switching during vascular disease [J]. Pflugers Arch, 2008, 456 (5): 769-785.
  • 5邓水秀,曾泗宇,任俊芳,郑元斌,廖端芳,秦旭平.降钙素基因相关肽对大鼠血管平滑肌细胞CDK2和Cyclin E的影响[J].中国临床药理学与治疗学,2011,16(3):249-253. 被引量:6
  • 6邓少雄,郭南鸥,郑渊,黄文森.替罗非班对急性ST段抬高型心肌梗死并糖尿病患者急诊经皮冠状动脉介入治疗术后血清MMP-9水平的影响及临床意义[J].中国临床药理学与治疗学,2011,16(7):807-811. 被引量:2
  • 7Khachigian LM. Early growth response-1 in cardio- vascular pathobiology[J]. Circ Res, 2006, 98 (2): 186-191.
  • 8Huang Z, Shi G, Gao F, et al. Effects of N-n-butyl haloperidol iodide on L-type calcium channels and intracellular free calium in rat ventricular myocytes [J]. Bioehem Cell Biol, 2007, 85(2) : 182-188.
  • 9Huang Z, Li H, Guo F, et al. Egr-1, the potential target of calcium channel blockers in cardioprotec- tion with ischemia/reperfusion injury in rats [J]. Cell Physiol Biochem, 2009, 24(1/2): 17-24.
  • 10Morishita R, Gibbons GH, Ellison KE, et al. Inti- mal hyperplasia after vascular injury is inhibited by antisense cdk 2 kinase oligonucleotides [J]. J Clin Invest, 1994, 93(4): 1458-1464.

二级参考文献31

共引文献6

同被引文献2

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部