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肿瘤坏死因子α和白细胞介素-1β可诱导原代培养的小鼠肝细胞表达血管细胞黏附分子-1,但干扰素γ不能。

Tumor necrosis factor alpha and interleukin-1 beta but not interferon gamma induce vascular cell adhesion molecule-1 expression on primary cultured murine hepatocytes.

作者信息

Watanabe Y, Morita M, Ikematsu N, Akaike T

机构信息

Department of Biomolecular Engineering, Tokyo Institute of Technology, Yokohama, Japan.

出版信息

Biochem Biophys Res Commun. 1995 Apr 6;209(1):335-42. doi: 10.1006/bbrc.1995.1508.

Abstract

Inflammatory cytokines such as tumor necrosis factor alpha (TNF alpha), interferon gamma (IFN gamma) and interleukin-1 beta (IL-1 beta) play important roles in the mechanisms of hepatitis. The effects of these cytokines on the expression of vascular cell adhesion molecule-1 (VCAM-1) in hepatocytes were examined. TNF alpha and IL-1 beta but not IFN gamma or IL-6 induced VCAM-1 expression on primary cultured murine hepatocytes in a dose- and a time-dependent fashion. TNF alpha is significantly more effective than IL-1 beta on the induction of VCAM-1 expression. The results of RT-PCR demonstrate that these cytokines regulate VCAM-1 expression at mRNA level. These results suggest that TNF alpha and IL-1 beta participate in the pathogenesis of hepatitis via induction of VCAM-1 molecules on hepatocytes.

摘要

炎性细胞因子,如肿瘤坏死因子α(TNFα)、干扰素γ(IFNγ)和白细胞介素-1β(IL-1β),在肝炎发病机制中发挥重要作用。研究了这些细胞因子对原代培养鼠肝细胞中血管细胞黏附分子-1(VCAM-1)表达的影响。TNFα和IL-1β而非IFNγ或IL-6以剂量和时间依赖性方式诱导原代培养鼠肝细胞上的VCAM-1表达。TNFα在诱导VCAM-1表达方面比IL-1β显著更有效。逆转录聚合酶链反应(RT-PCR)结果表明,这些细胞因子在mRNA水平调节VCAM-1表达。这些结果提示,TNFα和IL-1β通过诱导肝细胞上的VCAM-1分子参与肝炎的发病机制。

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