Sampaio E P, Sarno E N, Galilly R, Cohn Z A, Kaplan G
Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.
J Exp Med. 1991 Mar 1;173(3):699-703. doi: 10.1084/jem.173.3.699.
Thalidomide selectively inhibits the production of human monocyte tumor necrosis factor alpha (TNF-alpha) when these cells are triggered with lipopolysaccharide and other agonists in culture. 40% inhibition occurs at the clinically achievable dose of the drug of 1 micrograms/ml. In contrast, the amount of total protein and individual proteins labeled with [35S]methionine and expressed on SDS-PAGE are not influenced. The amounts of interleukin 1 beta (IL-1 beta), IL-6, and granulocyte/macrophage colony-stimulating factor produced by monocytes remain unaltered. The selectivity of this drug may be useful in determining the role of TNF-alpha in vivo and modulating its toxic effects in a clinical setting.
当人单核细胞在培养中被脂多糖和其他激动剂触发时，沙利度胺可选择性抑制人单核细胞肿瘤坏死因子α（TNF-α）的产生。在该药物临床可达到的1微克/毫升剂量下，抑制率达40%。相比之下，用[35S]甲硫氨酸标记并在SDS-PAGE上表达的总蛋白和单个蛋白的量不受影响。单核细胞产生的白细胞介素1β（IL-1β）、IL-6和粒细胞/巨噬细胞集落刺激因子的量保持不变。这种药物的选择性可能有助于确定TNF-α在体内的作用，并在临床环境中调节其毒性作用。
