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尼古丁通过调节核因子-κB激活来抑制U937细胞中炎症介质的产生。

Nicotine inhibits the production of inflammatory mediators in U937 cells through modulation of nuclear factor-kappaB activation.

作者信息

Sugano N, Shimada K, Ito K, Murai S

机构信息

Department of Periodontology, Nihon University School of Dentistry, 1-8-13 Kanda-Surugadai, Chiyoda-ku, Tokyo, 101-8310, Japan.

出版信息

Biochem Biophys Res Commun. 1998 Nov 9;252(1):25-8. doi: 10.1006/bbrc.1998.9599.

Abstract

Cigarette smoke is a major risk factor for lung cancer and respiratory infections. This increased susceptibility may result from cigarette smoke-induced impairment of the immune system. In this study, we evaluated the effect of nicotine on the production of inflammatory mediators by activated macrophages. Pretreatment with nicotine caused a significant inhibition of LPS-induced IL-1, IL-8, and PGE2 expression at the transcriptional level in U937 cells. Nicotine inhibited the activation of a transcription factor, NF-kappaB, which in turn, binds to and mediates transcriptional activation of these genes. These inhibitory effects of nicotine may contribute to cigarette smoke-induced immunosuppression.

摘要

香烟烟雾是肺癌和呼吸道感染的主要危险因素。这种易感性增加可能是由香烟烟雾引起的免疫系统损害所致。在本研究中,我们评估了尼古丁对活化巨噬细胞产生炎症介质的影响。尼古丁预处理导致U937细胞中脂多糖(LPS)诱导的白细胞介素-1(IL-1)、白细胞介素-8(IL-8)和前列腺素E2(PGE2)在转录水平上的表达受到显著抑制。尼古丁抑制了转录因子核因子κB(NF-κB)的活化,而NF-κB反过来又结合并介导这些基因的转录激活。尼古丁的这些抑制作用可能导致香烟烟雾引起的免疫抑制。

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