Watanabe Y, Morita M, Ikematsu N, Akaike T
Department of Biomolecular Engineering, Tokyo Institute of Technology, Yokohama, Japan.
Biochem Biophys Res Commun. 1995 Apr 6;209(1):335-42. doi: 10.1006/bbrc.1995.1508.
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.
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。
