克林霉素可调节脂多糖刺激的小鼠腹腔巨噬细胞中炎性细胞因子的诱导。
Clindamycin modulates inflammatory-cytokine induction in lipopolysaccharide-stimulated mouse peritoneal macrophages.
作者信息
Nakano Tetsuji, Hiramatsu Kazufumi, Kishi Kenji, Hirata Norio, Kadota Jun-Ichi, Nasu Masaru
机构信息
Second Department of Internal Medicine, Oita Medical University, Hasama, Oita 879-5593, Japan.
出版信息
Antimicrob Agents Chemother. 2003 Jan;47(1):363-7. doi: 10.1128/AAC.47.1.363-367.2003.
Abstract
We investigated the mechanism by which clindamycin (CLI) modulates cytokine induction after lipopolysaccharide (LPS) stimulation. Although CLI decreased the intracellular expression levels of tumor necrosis factor alpha and interleukin 1beta (IL-1beta) and increased IL-6 expression in macrophages, cytokine mRNA expression levels were similar in CLI-treated and untreated groups. Our findings suggest that CLI modulates cytokine production in LPS-stimulated macrophages.
摘要
我们研究了克林霉素（CLI）调节脂多糖（LPS）刺激后细胞因子诱导的机制。尽管CLI降低了肿瘤坏死因子α和白细胞介素1β（IL-1β）的细胞内表达水平，并增加了巨噬细胞中IL-6的表达，但CLI处理组和未处理组的细胞因子mRNA表达水平相似。我们的研究结果表明，CLI可调节LPS刺激的巨噬细胞中的细胞因子产生。
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本文引用的文献
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