摘要
目的 :观察 CD2 8在实验性自身免疫性肌炎 (EAM)发病中的作用 ;从 CD2 8核因子 κB(NFκB)信号传导通路探讨雷公藤多甙 (TWP)治疗多发性肌炎 (PM)的分子免疫学机制。方法 :用兔肌匀浆加等量完全福氏佐剂在大鼠背部肌肉和皮下组织多点注射制作 EAM动物模型。应用双色免疫荧光法流式细胞仪检测大鼠外周血 CD+ 4 和 CD+ 8T细胞上 CD2 8分子的表达 ;蛋白质免疫印迹 (Western blot)法检测 NFκB蛋白表达。结果 :EAM组外周血淋巴细胞以 CD+ 8T细胞为主 ,CD2 8及 NFκB表达明显增加。TWP组 CD+ 4 和 CD+ 8T细胞减少 ,CD2 8和 NFκB表达受抑制 (P<0 .0 5 )。结论 :EAM表现为 CD+ 8T细胞介导的细胞免疫反应异常 ,CD2 8在 EAM的发病中起重要作用 ,通过激活核转录因子使免疫反应进一步加强。 TWP可能通过抑制CD2 8NFκB这一信号传导通路从而抑制免疫反应。
Objective:To observe the role of CD28 in experimental autoimmune myositis (EAM) and explore the mechanism of tripterygium wilfordii polycoside(TWP) theatment.Methods:Twentyfour Wistar rats were randomly divided into three groups:normal saline(NS) group,EAM group,TWP group.By means of doublestained immunofluorscent flowcytometry the expression of CD28 were measured in CD+ 4 or CD+ 8 T lymphocyte.The expression of NFkappa B in nuclear protein were detected by westernblotting.Results:The percentage of CD+ 8 T lymphocyte were increased in EAM group,accompanied with the elevated expression of CD28 and nuclear factorkappa B(NFκB).However,in TWP group,the number of T lymphocytes and the expression of CD28 and NFκB were decreased significantly ( P<0.05 ).Conclusions:EAM is an CD+ 8 cytotoxic cells mediated immune disorder.CD28 might possess the effect of upregulating the immune response during the disease course,providing strong signals for activation of NFκB proteins.The treatment mechanism of TWP may be related to the suppression of CD28 singal transduction pathway.
出处
《中国中西医结合急救杂志》
CAS
2001年第4期198-201,共4页
Chinese Journal of Integrated Traditional and Western Medicine in Intensive and Critical Care
基金
国家自然科学基金资助项目 ( No.39870 90 9)
