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雌二醇对去卵巢实验性自身免疫性脑脊髓炎大鼠细胞间黏附分子-1及血脑屏障影响的研究 被引量:1

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摘要 目的探讨实验性自身免疫性脑脊髓炎(EAE)的发病机制和应用雌二醇治疗EAE的作用机制,为EAE和多发性硬化(MS)的免疫病理机制提供新的理论支持,也为今后临床应用雌激素辅助治疗MS等中枢神经系统(CNS)自身免疫性疾病提供实验依据。方法制备去卵巢后10d的EAE动物模型,随机分组。观察各组大鼠在不同时间的血清雌二醇水平及血清和脑脊液中白蛋白含量比值(QA),通过QA评定血脑屏障(BBB)的损害。评估临床症状,观察大鼠体质量变化、发病率等临床指标。免疫后(post-inoculation,p.i.)6、8、10、12、14、16d处死动物,取脑和脊髓用免疫组化技术检测CNS中不同部位细胞间黏附分子-1(ICAM-1)的表达,并对EAE组ICAM-1进行相关分析。结果雌二醇治疗组在发病率、体质量变化、症状评分、病灶数、发病时间明显低于EAE组,差异有统计学意义(P<0.05);3组大鼠在p.i.6、8、10、12、14、16dQA值比较,差异有统计学意义(P<0.05);3组大鼠在不同时间QA值达到高峰;3组大鼠在p.i.6dCNS内ICAM-1表达平均灰度比较,差异无统计学意义(P>0.05);3组大鼠在p.i.8、10、12、14、16dCNS内ICAM-1表达平均灰度比较,差异有统计学意义(P<0.05)。结论各组大鼠CNS内均可见ICAM-1的阳性表达,雌二醇治疗组ICAM-1表达明显低于EAE组,雌二醇对EAE的治疗可明显下调ICAM-1表达水平,减少BBB的损害。
出处 《实用心脑肺血管病杂志》 2010年第3期307-309,共3页 Practical Journal of Cardiac Cerebral Pneumal and Vascular Disease
基金 山西省2003年度回国留学人员科研基金资助项目(2003-69)
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  • 1Alt C, Duvefeh K, Franzen B, et al. Gene and Protein Expression Profiling of the Microvascular Compartment in Experimental Autoimmune Encephalomyelitis in C57B1/6 and SJL Mice [J]. Brain Pathology, 2005, 15 (1): 1-16.
  • 2Scott GS, Kean RB, Fabis MJ, et al. ICAM - 1 upregulation in the spinal cords of PLSJL mice with experimental allergic encephalomyelitis is dependent upon TNF - alpha production triggered by the loss of blood - brain barrier integrity [ J]. J Neuroimmunol, 2004, 155 (1/2) : 32 - 42.
  • 3Biemacki K, Prat A, Blain M, et al. Regulation of Cellulartes [ J]. J Neuropathol Exp Neurol, 2004, 63 (3) : 223 -232. and Molecular Trafficking across Human Brain Endothelial Cells by Th1 - and Th2- Polarized Lymphocy.
  • 4辛晋敏,马存根,梁丽云.实验性自身免疫性脑脊髓炎大鼠血-脑脊液屏障功能及动态变化[J].中国神经免疫学和神经病学杂志,2004,11(5):264-267. 被引量:12
  • 5Staykova M, Maxwell L, Willenborg D. Kinetics and polarization of the membrane expression of cytokine - induced ICAM - 1 on rat brain endothelial cells [J]. J Neuropathol Exp Neurol, 2000, 59 (2): 120- 128.
  • 6Bullard DC, Hu X, Schoeb TR, el al. Intercellular adhesion molecule - 1 expression is required on multiple celt types for the development of experimental autoimmune encephalomyelitis [ J ]. J Immunol, 2007, 178 (2): 851-857.
  • 7Carman CV, Springer TA. A transmigratory cup in leukocyte diapedesis both through individual vascular endothelial ceils and between them [J]. J Cell Biol, 2004, 167:377 -388.
  • 8Ma CG, Liu Y, Ma TH, et al. Monocyte ehemokine protein - 1 Mma expression in experimental allergic encephalomyelitis rats treated with or without triptolide [J]. J Neurol Sci, 2005, 238: 234.
  • 9辛晋敏,马存根,梁丽云,马太花,尉杰忠.细胞间黏附分子-1在实验性自身免疫性脑脊髓炎大鼠中表达的动态变化及作用[J].中国神经免疫学和神经病学杂志,2006,13(2):77-81. 被引量:10

二级参考文献18

  • 1[2]Juhler M. Pathophysiological aspects of acute experimental allergic encephalomyelitis [J]. Acta Neurol Scand Suppl, 1988,119:1-21.
  • 2[3]Ahn M,Kang J,Lee Y, et al. Pertussis toxin-induced hyperacute autoimmune encephalomyelitis in Lewis rats is correlated with increased expression of inducible nitric oxide synthase and tumor necrosis factor alpha[J]. Neurosci Lett, 2001,308 (1): 41-44.
  • 3[4]Goverman J,Brabb T. Rodent models of experimental allergic encephalomyelitis applied to the study of multiple sclerosis [J]. Lab Anim Sci, 1996,46 (5): 482-492.
  • 4[5]Dietrich JB. The adhesion molecule ICAM-1 and its regulation in relation with the blood-brain barrier[J].J Neuroimmunol, 2002,128(1-2): 58-68.
  • 5[6]Kitz K,Lassmann H,Karcher D, et al. Blood-brain barrier in chronic relapsing experimental allergic encephalomyelitis: a correlative study between cerebrospinal fluid protein concentrations and tracer leakage in the central nervous system [J]. Acta Neuropathol (Berl), 1984,63(1) :41-50.
  • 6[7]Lossinsky AS,Buttle KF,Pluta R, et al. Immunoultrastructural expression of intercellular adhesion molecule-1 in endothelial cell vesiculotubular structures and vesiculovacuolar organelles in blood-brain barrier development and injury[J]. Cell Tissue Res,1999,295 (1): 77-88.
  • 7[8]Wong D, Prameya R, Dorovini-Zis K. In vitro adhesion and migration of T lymphocytes across monolayers of human brain microvessel endothelial cells: regulation by ICAM-1 ,VCAM-1,E-selectin and PECAM1[J]. J Neuropathol Exp Neurol, 1999,58(2): 138-152.
  • 8[9]Namer IJ,Steibel J. Antibody directed against mannan of the Mycobacterium tuberculosis cell envelope provokes blood-brain barrier breakdown [J]. J Neuroimmunol, 2000,103 (1): 63-68.
  • 9Wong D, Prameya R, Dorovini-Zis K. In vitro adhesion and migration of T lymphocytes across monolayers of human brain microvessel endothelial eells: regulation by ICAM-1, VCAM-1, E-selectin and PECAM-1[J]. J Neuropathol Exp Neurol, 1999,58 (2) : 138-152.
  • 10Ahn M, Kang J, Lee Y. et al. Pertussis toxin-induced hyperacute autoimmune encephalomyelitis in Lewis rats is correlated with increased expression of inducible nitric oxide synthase and tumor necrosis factor alpha[J]. Neurosci Lett, 2001, 308(1):41-44.

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