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雷公藤内酯醇对EAE小鼠脊髓IL-10\IFN-γ表达的影响(1)
http://www.100md.com 2010年5月25日 任晓荣,樊红翠,尉杰忠,纪 宁,梁丽云,马存根
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     [摘要] 目的:观察雷公藤内酯醇(Tri)对实验性自身免疫性脑脊髓炎(EAE)小鼠模型临床症状和脊髓组织IL-10、IFN-γ的影响。方法:C57BL/6黑色小鼠随机分为EAE组、Tri治疗组及佐剂组,采用MOG35~55免疫动物建立EAE模型,治疗组腹腔注射Tri治疗,观察和评定小鼠临床症状,免疫组化染色观察脊髓中IL-10、IFN-γ的表达,并行相关图像分析。结果:EAE组与Tri治疗组发病时间、发病率等均有显著差异;与佐剂组比较,EAE组IFN-γ表达明显增高(P<0.01),IL-10表达降低(P<0.05);与EAE组比较,Tri治疗组IFN-γ表达降低(P<0.01),IL-10表达明显增加(P<0.05)。结论:Tri可明显改善EAE小鼠临床症状,其可能机制之一是通过抑制Th1及其分泌的IFN-γ,促进Th2及IL-10的分泌,调整Th1/Th2以治疗EAE。

    [关键词] 雷公藤内酯醇;多发性硬化;实验性自身免疫性脑脊髓炎;干扰素-γ;白介素-10

    [中图分类号] R332[文献标识码]A [文章编号]1673-7210(2010)05(c)-018-03

    Effects of Triptolide on IL-10 and IFN-γ in spinal cord of EAE mice

    REN Xiaorong1, FAN Hongcui1, YU Jiezhong2, JI Ning2, LIANG Liyun2, MA Cungen2

    (1.Department of Neurology, the First Clinical Medical College of Shanxi Medical University, Taiyuan030001, China; 2.Institiute of Brain Science, Shanxi Datong University, Datong 037000, China)

    [Abstract] Objective: To observe the effects of Triptolide (Tri) on IL-10 and IFN-γ in spinal cord of EAE mice. Methods: C57BL/6 mice were randomly divided into EAE group, Tri treatment group and adjuvant group. EAE model was established with MOG35-55, Tri was intraperitoneally injected in treatment group. The symptoms of mice in EAE were monitored according to the international standard of 5-scores-system. The spinal cord was used for IL-10, IFN-γ immunohistochemical staining. Results: The differences of incidence, change of body weight and mean maximum clinical scores between EAE group and Tri treatment group were statistically significant (P<0.05). After the intervention of Tri, compared with adjuvant group, the level of IFN-γ in EAE group was increased (P<0.01), and the level of IL-10 was decreased (P<0.05). Compared with EAE group, IFN-γ in Tri group was decreased (P<0.01), and the level of IL-10 was significantly increased (P<0.05). Conclusion: Tri can treat EAE mice effectively. It may be caused by depressing IFN-γ secreted by Th1 and promoting IL-10 secreted by Th2, which can regulate Th1/Th2.

    [Key words] Triptolide; Multiple sclerosis; Experimental autoimmune encephalomyelitis; IFN-γ; IL-10 ......

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