γ-干扰素加肿瘤坏死因子-α对小鼠胰岛细胞中一氧化氮及一氧化氮合酶mRNA的诱导作用

Nitric oxide and nitric oxide synthase mRNA induction in mouse islet cells by interferon-gamma plus tumor necrosis factor-alpha.

作者信息

Yamada K, Otabe S, Inada C, Takane N, Nonaka K

机构信息

Department of Medicine, Kurume University School of Medicine, Fukuoka, Japan.

出版信息

Biochem Biophys Res Commun. 1993 Nov 30;197(1):22-7. doi: 10.1006/bbrc.1993.2435.

DOI:10.1006/bbrc.1993.2435

PMID:7504484

Abstract

It has been shown that nitric oxide (NO) is involved in islet cell damage induced by interleukin-1 (IL-1). Here we show that interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) synergistically induced NO production and inducible NO synthase (iNOS) mRNA expression in mouse islet cells. Cycloheximide (CXH) did not prevent the iNOS mRNA expressions. The combination of IFN-gamma and TNF-alpha, which is highly cytotoxic to mouse islet cells, failed to destruct islet cells in the absence of L-arginine or in the presence of NG-monomethyl-L-arginine (NMMA). These observations suggest that NO is a primary effector in islet cell damage caused by IFN-gamma plus TNF-alpha.

摘要

已表明一氧化氮（NO）参与白细胞介素-1（IL-1）诱导的胰岛细胞损伤。在此我们表明，干扰素-γ（IFN-γ）和肿瘤坏死因子-α（TNF-α）协同诱导小鼠胰岛细胞中NO的产生和诱导型一氧化氮合酶（iNOS）mRNA的表达。放线菌酮（CXH）不能阻止iNOS mRNA的表达。对小鼠胰岛细胞具有高度细胞毒性的IFN-γ和TNF-α的组合，在缺乏L-精氨酸或存在NG-单甲基-L-精氨酸（NMMA）的情况下未能破坏胰岛细胞。这些观察结果表明，NO是IFN-γ加TNF-α引起的胰岛细胞损伤中的主要效应因子。