雷公藤多苷对自身免疫性甲状腺炎大鼠模型外周血CXCR3、CCR4基因表达的影响  

Impact of tripterygium glycosides on the expression of CXCR3 and CCR4 genes in peripheral blood from experimental autoimmune thyroiditis rats

作　　者：徐晓光[1] 张红[2] 顾军[1] 

机构地区：[1]第二军医大学长海医院皮肤科,上海200433 [2]青岛海慈医疗集团皮肤科

出　　处：《中华皮肤科杂志》2010年第11期792-795,共4页Chinese Journal of Dermatology

摘　　要：目的分析雷公藤多苷对实验性自身免疫性甲状腺炎大鼠外周血单一核细胞中CXCR3、CCR4基因表达的影响，探讨其调节Th1／Th2平衡的可能机制。方法清洁级雌性Wistar大鼠20只，建立实验性自身免疫性甲状腺炎动物模型，随机分成两组，对照组与雷公藤组，分别每天给予生理氯化钠溶液、雷公藤多苷片悬液5．5mg／kg灌胃治疗。4周后处死大鼠，提取外周血单一核细胞，抽提RNA并反转录成cRNA，以Thl—Th2一Th3微点阵基因芯片及实时RT—PCR方法检测CXCR3、CCR4基因表达差异。结果与实验性自身免疫性甲状腺炎大鼠对照组相比较，雷公藤多苷片治疗组外周血单一核细胞中CXCR3表达明显下降（雷公藤多苷片组和对照组分别为0．52±0．10和1．05±0．17，P〈0．01），而CCR4明显升高（分别为1．56±0．13和1．02±0．09，P〈0．01），CXCR3／CCR4比值明显低于对照组（分别为0．39±0．22和1．04±0．12，P〈0．01）。结论雷公藤多苷可能通过降低CXCR3、升高CCR4来调节实验性自身免疫性甲状腺炎大鼠体内Th1、Th2细胞及其细胞因子的比例，从而达到调节Th1／Th2平衡的目的。Objective To analyze the impact of tripterygium glycosides （TG） on the expression of CXCR3 and CCR4 gene in peripheral blood mononuclear cells from experimental autoimmune thyroiditis （EAT） rats, and to explore the possible mechanism for regulation of Thl/Th2 balance by TG. Methods EAT was induced in 20 rats, which were randomly divided into two groups, i.e., control group and TG group, to receive intragastric physiological saline and TG suspension （5.5 mg/kg） daily, respectively. The rats were killed 4 weeks later, and total RNA was extracted from the peripheral blood mononuelear cells of rats and used for cRNA synthesis. The gene expressions of CXCR3 and CCR4 were detected with a Th1-Th2-Th3 microarray gene chip and reahime RT-PCR. Results Compared with the control group, there was a significant decrease in the mRNA expression of CXCR3 （0.52 ± 0.10 vs. 1.05 ±0.17, P 〈 0.01） and CXCR3/CCR4 ratio （0.39 ±0.22 vs. 1.04±0.12, P 〈 0.01） in the TG group, together with an increase in the mRNA expression of CCR4 （1.56 ± 0.13 vs. 1.02±0.09, P 〈 0.01 ）. Conclusions TG could regulate the number of Thl and Th2 cells as well as their cytokine expression ratio likely by reducing CXCR3 and enhancing CCR4 expression, so as to modulate the Th1/Th2 balance in EAT rats.

关 键 词：雷公藤属 甲状腺炎 自身免疫性 THL细胞 Th2细胞 炎症趋化因子类 疾病模型 动物 

分 类 号：R285.5[医药卫生—中药学]