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机构地区:[1]上海徐汇区大华医院皮肤科,上海200237 [2]第二军医大学长海医院皮肤科,上海200433 [3]青岛市海慈医疗集团皮肤科,山东青岛266033 [4]张家港澳洋医院皮肤科,江苏张家港215600
出 处:《中国皮肤性病学杂志》2011年第7期521-523,572,共4页The Chinese Journal of Dermatovenereology
摘 要: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 impact of thalidomide on expression of CXCR3 and CCR4 in peripheral blood of ex- perimental autoimmune thyroiditis (EAT) rats, and to explore its possible mechanism in regulating Thl/Th2 balance. Methods EAT models were established in 20 female Wistar rats,which were then randomly divided into two groups: control model group and thalidomide group. Another 10 rats were set as normal group. Rats of normal and control model groups were given normal saline by garage per day, while thalidomide group were given thalidomide suspension 6.875mg/kg per day for four weeks. Then rats were killed, serum were collected and total RNA of peripheral blood mononuclear cells was extracted, levels of CXCR3 and CCR4 were detected by Thl-Th2-Th3 Microarray gene chip,realtime RT-PCR and ELISA methods respectively. Results Compared with the normal group,the expression of CXCR3 was increased in peripheral blood of model group,and CX- CR3/CCR4 ratio increased too,while CCR4 declined obviously (P 〈 0.01 ). After treatment with thalidomide, the expressions of both CXCR3 and CCR4 were decreased, and the ratio of CXCR3/CCR4 was decreased too (all P 〈 0.01 ). Conclusion Thalidomide might depress the expressions of both CXCR3 and CCR4, espe- cially to gene CXCR3, so as to regulate the number of Thl and Th2 cells and their cytokines to achieve the purpose of regulating Th1/Th2 balance in EAT rats.
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