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目的分析沙利度胺对实验性自身免疫性甲状腺炎大鼠外周血中CXCR3和CCR4表达的影响,探讨其调节Th1/Th2平衡的可能机制。方法用20只清洁级雌性Wistar大鼠建立实验性自身免疫性甲状腺炎动物模型,并将其随机分成两组,即模型对照组与沙利度胺组;另取10只清洁级雌性Wistar大鼠不作预处理,将其设为正常对照组。正常对照组及模型对照组大鼠每天给予生理盐水灌胃,沙利度胺组大鼠给予沙利度胺片悬液6.875mg/(kg.d)灌胃处理,4周后处死大鼠,采集血清,同时提取外周血单核细胞,以Th1-Th2-Th3Microarray基因芯片、realtime RT-PCR和ELISA法检测其CXCR3和CCR4基因及蛋白水平差异。结果与正常对照组相比,模型对照组大鼠外周血CXCR3和CXCR3/CCR4比值升高,CCR4明显下降;而经沙利度胺处理后,其CXCR3和CCR4表达均下降,CXCR3/CCR4比值也明显降低,差异均有统计学意义(P均<0.01)。结论沙利度胺可同时下调CXCR3和CCR4的表达,以CXCR3为甚,从而诱导实验性自身免疫性甲状腺炎大鼠体内不同Th细胞的迁移,在一定程度上起到辅助调节Th1/Th2平衡的作用。
Objective To analyze the effect of thalidomide on the expression of CXCR3 and CCR4 in peripheral blood of experimental autoimmune thyroiditis rats and to explore the possible mechanism of its regulation of Th1 / Th2 balance. Methods Twenty experimental female Wistar rats were used to establish experimental autoimmune thyroiditis animal models and randomly divided into two groups: model control group and thalidomide group. Another 10 female Wistar rats Without pretreatment, set it as normal control group. Rats in normal control group and model control group were given normal saline daily. Thalidomide rats were administrated with thalidomide suspension 6.875mg / (kg.d) orally, and rats were killed after 4 weeks. The serum was collected and the peripheral blood mononuclear cells were extracted simultaneously. The gene and protein levels of CXCR3 and CCR4 were detected by Th1-Th2-Th3Microarray microarray, realtime RT-PCR and ELISA. Results Compared with the normal control group, the ratio of CXCR3 and CXCR3 / CCR4 in peripheral blood of model control group increased and CCR4 decreased significantly. After thalidomide treatment, the expression of CXCR3 and CCR4 decreased, and the ratio of CXCR3 / CCR4 Significantly lower, the difference was statistically significant (P all <0.01). Conclusions Thalidomide can down-regulate the expression of CXCR3 and CCR4 simultaneously, especially in CXCR3, so as to induce the migration of different Th cells in experimental autoimmune thyroiditis rats and to some extent help to regulate the Th1 / Th2 balance effect.