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目的:研究雷公藤多苷对IgA肾病(IgAN)大鼠外周血γδT细胞分布及表达转化生长因子β1(TGF-β1)功能的影响。方法:复制IgAN大鼠模型,并予雷公藤多苷干预治疗,同时给予泼尼松对照,运用流式细胞仪检测各组用药前后外周血γδT细胞比率、放射免疫法检测血清IgA水平;以抗TCRγδ单克隆抗体(mAb)固相法,体外选择性地扩增γδT细胞。在体外培养的条件下,以抗CD3抗体刺激48h后,用ELISA法测定培养体系中TGF-β1的表达。结果:雷公藤多苷能抑制血清IgAN外周血γδT细胞与血清IgA的升高,同时还能抑制γδT分泌TGF-β1的过度分泌。结论:通过降低血清IgAN外周血γδT细胞与血清IgA水平,同时抑制γδT分泌TGF-β1的过度分泌,可能是雷公藤多苷治疗IgAN的作用机制之一。
Objective: To study the effects of tripterygium glycosides on the distribution of peripheral blood γδT cells and the expression of transforming growth factor β1 (TGF-β1) in rats with IgA nephropathy (IgAN). METHODS: IgAN rat model was duplicated and treated with Tripterygium glycosides. Prednisone control was used. Flow cytometry was used to detect the ratio of γδ T cells in peripheral blood before and after administration, and radioimmunoassay was used to detect serum IgA level. The solid phase method of TCRγδ monoclonal antibody (mAb) was used to selectively amplify γδT cells in vitro. Under the condition of in vitro culture, the expression of TGF-β1 in the culture system was measured by ELISA after 48 h stimulation with anti-CD3 antibody. RESULTS: Tripterygium glycosides inhibited the increase of serum IgAN γδT cells and serum IgA, and also inhibited the secretion of TGF-β1 secreted by γδT. Conclusion: It may be one of the mechanisms of the treatment of IgAN by glycosides of glycosides by lowering the serum IgAN γδT cells and serum IgA levels and inhibiting the secretion of TGF-β1 secreted by γδT.