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实验性变态反应性脑脊髓炎大鼠穹窿下器凋亡细胞的观察 被引量：2

Morphological study of the apoptotic cells on the subfornical organ of rats with experimental allergic encephalomyelitis
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摘要 目的通过观察实验性变态反应性脑脊髓炎(EAE)大鼠不同时期下穹窿下器(SFO)凋亡细胞的变化,进一步探讨该室周器官在EAE发病过程中的意义。方法建立大鼠EAE模型,利用TUNEL技术来观察大鼠SFO在EAE不同时期细胞凋亡的改变。结果SFO的凋亡细胞在EAE 6小时、EAE 7天、EAE 14天、EAE 21天分别为(13.67±2.31)、(19.33±2.08)、(24.67±6.79)、(9.33±1.76),而对照组为(5.33±2.52)。与对照组比较,EAE 6小时、7天、14天组细胞凋亡数明显增加(P<0.05),EAE 21天组无显著差异(P>0.05)。结论SFO在EAE的不同时期凋亡细胞的变化与临床进展呈一致性,可能是血携免疫分子早期入脑的位点。 Objective To observe the apoptotic cells on the subfornical organ of rats in different periods of experimental allergic encephalomyelitis, and to study the significance of SFO in EAE. Methods Animal models were actively immunized to induce EAE. Then their subfornical organs were taken out to observe in different periods by TUNEL histochemistry. Results The number of apoptosis cells of SFO is （ 13.67 ± 2.31 ） at 6 hours after EAE, （19.33±2.08） at 7day after EAE, （24.67 ±6.79） at 14 day after EAE, （9.33 ± 1.76） at 21day after EAE, （5.33 ± 2.52） in control group . The number increased significantly at 6 hours ,7 day, 14 day after EAE compared with that in control group （ P 〈 0.05 ）, not significantly at 21 day after EAE （ P 〉 0.05 ）. Conclusion The change of apoptosis cells of SFO is consistent with process of EAE, maybe it is the entry sites of blood borne immune messages into the brain.
作者 叶建亚
机构地区 石家庄卫生学校
出处 《脑与神经疾病杂志》 2009年第5期339-341,共3页 Journal of Brain and Nervous Diseases
基金 河北省自然科学基金项目(302491)
关键词 实验性变态反应性脑脊髓炎 穹窿下器 凋亡细胞 大鼠 Experimental allergic encephalomylitis Subfornical organ Apoptotic cells Rats
分类号 R744.5 [医药卫生—神经病学与精神病学]
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参考文献12

  • 1Petry KG, Boulleren AI, Pousset F, et al. Experimental allergic encephalomyelitis animal models for analyzing features of multiple sclerosis. Pathol Biol ( Paris), 2000, 48 : 48-53.
  • 2Nguyen KB, McCombe PA, Pender MP. Macrophage apoptosis in the central nervous system in experimental autoimmune encephalomyelitis. J Autoimmun, 1994, 7: 145-152.
  • 3Pender MP. Activation-induced apoptosis of autoreactive and alloreactive T lymphocytes in the target organ as a major mechanism of tolerance . Immunol Cell Biol, 1999, 77 : 216-223.
  • 4Suvannavejh GC, Dal Canto MC, Matis LA, et al. Fas-mediated apoptosis in clinical remissions of relapsing experimental autoimmune encephalomyelitis. J Clin Invest, 2000, 105: 223-231.
  • 5孟荔 欧阳建.凋亡与自身免疫病的研究进展.中外健康文摘(医药学刊),2007,4(9):31-32.
  • 6Tabi Z, Mcombe PA, Pender MP. Antigen-specific down-regulation of myelin basic protein-reactive T ceils during spontaneous recovery from experimental autoimmune encephalomyelitis: further evidence of apoptotic deletion of autoreactive T ceils in the central nervous system. Int Immunol, 1995, 7 : 967-973.
  • 7Okuda Y, Bernard CC, Fujimura H, et al. Fas has a crucial role in the progression of experimental autoimmune encephalomyelitis. Mol Immunol, 1998, 35 : 317-326.
  • 8王惠,林嘉友,杨天祝.实验性变态反应性脑脊髓炎与细胞凋亡[J].中国神经免疫学和神经病学杂志,2000,7(3):175-179. 被引量：4
  • 9Quan N, Stern EL, Whiteside MB, et al. Induction of pro-inflammatory cytokine mRNAs in the brain after peripheral injection of subseptic doses of lipopolysaccharide in the rat. J Neuroimmunol, 1999,93 : 72 -80.
  • 10White CA, McCombe PA, Pender MP. The roles of Fas, Fas ligand and Bcl-2 in T cell apoptosis in the central nervous system in experimentral autoimmune encephalomyelitis. J Neuroimmunol, 1998, 82 : 47-55.

二级参考文献38

  • 1[1] Zielasek J, Jung S, Gold R, et al. Adm inistration of nitric oxide synth ase inhibitors in experimental autoimmune neuritis and experimental autoimmun e encephalomyelitis[J]. J Neuroimmunol, 1995,58:81-88.
  • 2[2] Cross AH, Misko TP, Lin RF, et al. Aminoguanidi ne, an inhibitor of indu cible nitric oxide synthase, ameliorates experimental autoimmune encephalomyelit is in SJL mice[J]. J Clin Invest, 1994,93:2684-2690.
  • 3[3] Sabelko KA, Kelly KA, Nahm MH, et al. Fas and Fas ligand enhance the pathogensis of experimental allergic encephalomyelitis, but are not essential fo r immune privilege in the central nervous system[J]. J Immunol, 1997,159 :3096-3099.
  • 4[4] Waldner H, Sobel RA, Howard E, et al. Fas- and Fas-L-deficient mice are resistant to induction of autoimmune encephalomyelitis[J]. J Immunol, 1997,159:3100-3103.
  • 5[5] Okuda Y, Bernard CCA, Fujimura H, et al. Fas ha s a crucial role in the progression of experimental autoimmune encephalomyelitis[J]. Mol Immunol, 1998 ,35(5):317-326.
  • 6[6] D`Souza SD, Bonetti B, Balasingam V, et al. Mul tiple slcerosis: Fas si gnaling in oligodendrocyte cell death[J]. J Exp Med, 1996,184:2361-237 0.
  • 7[7] Nguyen KB, McCombe PA，Pender MP. Macrophage apopt osis in the central n ervous system in experimental autoimmune encephalomyelitis[J]. J Autoimmun, 1994,7:145-152.
  • 8[8] Bonetti B, Pohl J, Gao YL, et al. Cell death du ring autoimmune demyeli nation:effector but not target cells are eliminated by apoptosis[J]. J Immun ol, 1997,159:5733-5741.
  • 9[9] Tabi Z, McCombe PA，Pender MP. Apoptic elimination of Vβ 8.2+ cells f rom the central nervous system during recovery from experimental autoimmune enc ephalitogenic T cells[J]. Eut J Immunol, 1994,24:2609-2617.
  • 10[10] McCombe PA, Nickson I, Tabi Z, et al. Apoptosis of V beta 8.2+ T ly mphocytes in the spinal cord during recovery from experimental autoimmune encep halomyelitis induced in Lewis rats by inoculation with myelin basic protein K[ J]. Neurol Sci, 1996,139(1):1-6.

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脑与神经疾病杂志
2009年 第5期

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