地塞米松对巨噬细胞信号转导接头蛋白MyD88的抑制作用  

Inhibitory effect of dexamethasone on myeloid differentiation factor 88 and tumor necrosis factor-α expressions in mouse peritoneal macrophages

作　　者：赵文杰[1,2] 席丽艳[1] 马黎[1] 张军民[1] 李希清[1] 鲁长明[1] 李飞[3] 

机构地区：[1]中山大学附属第二医院皮肤科,广东广州510120 [2]福建中医学院附属厦门中医院皮肤科,福建厦门361009 [3]中山大学附属中山市人民医院心血管科,广东中山528400

出　　处：《南方医科大学学报》2009年第12期2404-2406,2409,共4页Journal of Southern Medical University

基　　金：国家自然科学基金(30770121)

摘　　要：目的研究地塞米松对马尔尼菲青霉固有免疫反应中巨噬细胞信号转导接头蛋白MyD88的作用。方法马尔尼菲青霉酵母相菌液与小鼠腹腔巨噬细胞共培养,应用地塞米松作用后采用ELISA法测定培养液上清中TNF-α的浓度;Real time PCR及Western blot法检测MyD88的蛋白及基因表达。结果地塞米松抑制被马尔尼菲青霉激活的巨噬细胞产生TNF-α,并抑制巨噬细胞接头蛋白MyD88的蛋白及mRNA的表达。结论地塞米松对马尔尼菲青霉固有免疫反应抑制作用与其对MyD88的抑制相关。Objective To study the inhibitory effect of dexamethasone （DEX） on myeloid differentiation factor 88 （MyD88） and tumor necrosis factor-α （TNF-α） expression in mouse peritoneal macrophages in innate immune response to Penicillium marneffei （PM）. Methods Mouse peritoneal macrophages were cultured in the presence of heat-inactivated yeast-phase PM with or without DEX, and the protein and mRNA expressions of MyD88 in the macrophages were detected using Western blotting and real-time PCR, respectively. TNF-α in the cell culture supernatant was measured with enzyme-linked immunosorbent assay. Results DEX suppressed TNF-α production by the macrophages co-cultured with PM. The expressions of MyD88 were up-regulated by PM stimulation, whose effect was inhibited by the application of DEX. Conclusion The inhibitory effect of DEX on PM-induced proinflammatory responses of the macrophage is directly associated with the inhibition of MyD88 expression.

关 键 词：地塞米松 髓样分化蛋白88 马尔尼菲青霉 巨噬细胞 肿瘤坏死因子Α 

分 类 号：R96[医药卫生—药理学]