换一批Thalidomide inhibits lipopolysaccharide-induced tumor necrosis factor-alpha production via down-regulation of MyD88 expression.
第一作者：
Abu Shadat M,Noman
第一单位：
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan.
作者：
医学主题词
动物(Animals);细胞系(Cell Line);细胞, 培养的(Cells, Cultured);半胱氨酸蛋白酶抑制剂(Cysteine Proteinase Inhibitors);减量调节(Down-Regulation);I-κB蛋白质类(I-kappa B Proteins);免疫抑制剂(Immunosuppressive Agents);白细胞介素1受体相关激酶类(Interleukin-1 Receptor-Associated Kinases);JNK丝裂原活化蛋白激酶类(JNK Mitogen-Activated Protein Kinases);亮肽菌素类(Leupeptins);脂多糖类(Lipopolysaccharides);巨噬细胞(Macrophages);小鼠(Mice);小鼠, 近交BALB C(Mice, Inbred BALB C);髓样分化因子88(Myeloid Differentiation Factor 88);NF-κB(NF-kappa B);磷酰化(Phosphorylation);蛋白酶体内肽酶复合物(Proteasome Endopeptidase Complex);原癌基因蛋白质c-akt(Proto-Oncogene Proteins c-akt);TNF受体相关因子6(TNF Receptor-Associated Factor 6);沙立度胺(Thalidomide);Toll样受体2(Toll-Like Receptor 2);Toll样受体4(Toll-Like Receptor 4);肿瘤坏死因子α(Tumor Necrosis Factor-alpha);p38丝裂原活化蛋白激酶类(p38 Mitogen-Activated Protein Kinases)
DOI
10.1177/1753425908099317
PMID
19201823
发布时间
2017-11-16
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Innate immunity
33-41页
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