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针刺对帕金森病模型大鼠血液T淋巴细胞亚群的影响 被引量:3

Effect of acupuncture on blood T lymphocyte subpopulation in rat model with Parkinson's disease
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摘要 目的:探讨针刺治疗对帕金森模型大鼠T淋巴细胞亚群的影响。方法:采用脑内黑质部注射6-羟基多巴制备帕金森病大鼠模型,分别采用针刺、美多巴及针刺结合美多巴对模型大鼠进行治疗。采用免疫荧光法测定T细胞亚群数。结果:CD3,CD4,CD8在正常对照组为(68.7±8.8)%,(42.1±8.0)%,(31.4±6.4)%;模型自然恢复组为(54.9±8.4)%,(31.9±7.8)%,(23.9±4.2)%;针刺治疗组为(66.8±8.7)%,(32.1±9.9)%,(29.9±6.6)%;美多巴治疗组为(68.4±7.3)%,(31.9±5.4)%,(31.2±7.6)%;针刺结合美多巴治疗组为(69.3±7.6)%,(32.8±8.0)%,(32.3±6.3)%。与正常对照组比较,模型自然恢复组CD3,CD4,CD8均明显降低(t=1.814~1.831,P<0.05)。与模型自然恢复组比较,针刺、美多巴及针刺结合美多巴治疗后CD3,CD8的百分数明显升高(t=1.813~1.830,P<0.05)。结论:针刺治疗帕金森病模型大鼠有效可能与调节T淋巴细胞亚群的比例及改善其功能有关。 AIM:To investigate the effect of acupuncture on blood T lymphocyte subgpopulation in rat model with Parkinson's disease(PD). METHODS:PD models of rats were established by injecting 6 OHDA into substantia nigra.Acupuncture,medopa,and combination of acupuncture and medopa were used to treat the model rats respectively.The amount of T lymphocyte subpopulations was determined with immunofluorescence method. RESULTS:The percentages of CD3, CD4 and CD8 were(68.7±8.8)%, (42.1±8.0)%and(31.4±6.4)%for the control group,(54.9±8.4)%,(31.9±7.8)%and(23.9±4.2)%for the model group, (66.8±8.7)%,(32.1±9.9)%and(29.9±6.6)%for the acupuncture group,(68.4±7.3)%,(31.9±5.4)%and(31.2±7.6)%for the medopa group,and(69.3±7.6)%,(32.8±8.0)%and(32.3±6.3) for the therapeutic alliance group.Compared with the control group, the percentages of CD3, CD4,CD8 were obviously decreased in the model group(t=1.814-1.831,P< 0.05).Compared with the model group, the percentages of CD3,CD8 were significantly increased in the three treatment groups (t=1.813-1.830, P< 0.05). CONCLUSION:Curative effect of acupuncture in the treatment of PD may be related with the regulation of the ratio of T lymphocytes' subgroups and its functional improvement.
出处 《中国临床康复》 CSCD 2004年第10期1904-1905,共2页 Chinese Journal of Clinical Rehabilitation
基金 广东省中医药管理局资助项目(101112) 深圳市科委资助项目(F2000A20)~~
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参考文献17

  • 1郑国庆,蔡业峰,雒晓东,黄燕,黄培新.帕金森病的综合性治疗[J].中国临床康复,2002,6(15):2234-2235. 被引量:12
  • 2Perese DA, Ulman J, Viola J, et aI. 6-hydroxydopamine-induced selective parkinsonian rat model. Brain Res 1989; 494:285.
  • 3Thomas J, Wang J, Takubo H, et al. 6-hydroxydopamine-induced selective parkinsonian rat model: further biochemical and behavioral characterization. Exp Neurol 1994; 126:159.
  • 4Pellegrino LJ, Pellegrlno AS, Cushman AJ. A stereotaxic atlas of the rat brain. 2^nd edition, Plenum press 1979:43.
  • 5Kluter H, Vieregge P, Stolzer H, et al. Defective production of interleukin-2 in patients with idiopathic Parkinson disease. J Neurol Sci 1995; 133( 1 - 2): 134.
  • 6Bessler H, Djaldetti R, Salman H, et al. IL-1 beta, IL-2, IL-6 and TNF-alpha production by peripheral blood mononuclear cells from patients with Parkinson disease. Biomed Pharmacother 1999; 53(3): 141.
  • 7Fiszer U, Mix E, Fredrik.son S, et al. Gama delta + T cell are increased in patients with Parkinson disease. J Neurol Sci 1994; 121:39.
  • 8Bokor M, Fao A, Schnabel R, et al. Relationship between the immune system and the diseases of the central nervous system. Ther Hung 1992; 40(2) : 51.
  • 9孙业红,李东,王森,胡刚.帕金森病治疗中的机制认识[J].中国临床康复,2003,7(5):792-793. 被引量:10
  • 10李文昌,邓建中,昝慧敏,曹明芳.Analysis of immunological changes in 36 patients with Parkinson's disease[J].中国临床康复,2002,6(19):2972-2972. 被引量:5

二级参考文献18

  • 1[1]Joseph J. Levodopa strengths and weaknesses. Neurology 2002; 58(4 Suppl 1):19 -32
  • 2[2]Ball J. Current advances in Parkinson's disease. Trends Neuronsci 2001; 24(7):367 - 9
  • 3[3]Douglas C, Wallace. Mouse Models for Mitochondrial Disesse. Semin Med Genet 2001; 106:71-93
  • 4[4]Beal MF. Energetics in the pathogenesis of neurodegenerative diseases . Trends in Neuroscience 2000; 23:298 - 304
  • 5[5]Birgit L, Jochen R. Molecular physiology of neuronal K-ATP channels(Review) .Molecular Membrane Biology 2001; 18:117-27
  • 6[6]Paik SR, Shin HJ, Lee JH. Metal-catalyzed oxidation of alpha-synuclein in the presence of copper ( Ⅱ ) and hydrogen peroxide . Arch Biochem Biophys 2000;378:269 - 77
  • 7[7]Blandini, Nappi G, Tassorelli C, Martignoni E. Functional change of the basal ganglia circuity in Parkinsnn' s disease. Prog Neurobiol 2000; 62 ( 1 ): 63 - 88
  • 8[8]David B, Sakina T, Nathalie L, et al. Molecular pathways involved in the neurotoxicity of 6-OHDA, dopamine and MPTP: contribution to the apoptotic theory in Parkinson's disease. Prog Neurobiol 2001; 65:135 -72
  • 9[9]Vilab M, Jackson-Lewis V, Guegan C, et al. The role of glial cells in Parkinson' s disease. Curr opin Neurol 2001; 14(4):483 -9
  • 10[10]Clayton PT, Smith I, Harding B, et al. Subacute combined degeneration of the cord, dementia and parkinsonism due to an inborn error of folate metabolism. J Neurosury Psychiatry 1986; 49:920-7

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