摘要
目的 探讨协同刺激分子在实验性变态反应性神经炎 (EAN)发病中的作用及雷公藤多甙的影响。方法 用兔坐骨神经匀浆免疫小鼠建立EAN模型 ,雷公藤多甙 (TWP)灌胃治疗 ,观察小鼠发病情况和病理改变 ;通过流式细胞计检测小鼠外周血淋巴细胞CD2 8、CTLA 4、B7 1、B7 2蛋白的表达 ;用RT PCR检测外周血淋巴细胞B7 1和B7 2mRNA的表达。结果 EAN小鼠外周血淋巴细胞上协同刺激分子CD2 8、CTLA 4、B7 1、B7 2蛋白的表达水平明显增高 ,B7 1和B7 2mRNA表达与蛋白的增加相平行。雷公藤多甙治疗组的发病率及病变程度均明显降低 ,同时伴随CD2 8、B7 1、B7 2蛋白的表达及B7 1、B7 2、mRNA表达的水平降低。结论 协同刺激分子的表达对T细胞活化起重要作用 ;雷公藤多甙能减轻ENA的病变程度 ,可能与抑制了B7 1及B7 2的基因转录或转录以上环节和抑制了CD2 8翻译或翻译以上环节有关。
Objective To investigate the roles of costimulatory molecules in experimental allergic neuritis(EAN) and the mechanism of Tripterygium Wilfordii polypeptide(TWP) treatment. Methods The protein expression of CD28/CTLA 4: B7 1/B7 2 in T lymphocyte was measured with flow cytometry and the mRNA expression of B7 1 and B7 2 with reverse transcription polymerase chain reaction(RT PCR).Results After TWP treatment, the expression of CD28: B7 1/B7 2 decreased greatly, the differences were marked ( P < 0.01 ), the incidence and severity of EAN were significantly reduced. The expression of B7 1 and B7 2 mRNA was positively correlative with that of B7 1 and B7 2 protein respectively. Conclusion The results indicated that CD28/CTLA 4: B7/B7 2 play a pivotal role in the EAN. The suppressive effect of TWP on EAN was associated with the restrain of procedures from gene to mRNA in B7 1 and B7 2, and from mRNA to protein in CD28.
出处
《卒中与神经疾病》
2001年第2期67-70,共4页
Stroke and Nervous Diseases
基金
国家自然科学基金 (No .3 9870 90 9)资助
