Morikawa Akiko, Koide Naoki, Sugiyama Tsuyoshi, Mu Mya Mya, Hassan Ferdaus, Islam Shamima, Ito Hiroyasu, Mori Isamu, Yoshida Tomoaki, Yokochi Takashi
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan.
FEMS Immunol Med Microbiol. 2004 Jul 1;41(3):211-8. doi: 10.1016/j.femsim.2004.03.008.
The effect of D-galactosamine (D-GalN) on nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells was examined. D-GalN augmented the production of NO, but not tumor necrosis factor (TNF)-alpha in LPS-stimulated RAW 264.7 cells. Pretreatment of D-GalN augmented the NO production whereas its post-treatment did not. D-GalN augmented the NO production in RAW 264.7 cells stimulated with either TNF-alpha and interferon-gamma. The augmentation of LPS-induced NO production by D-GalN was due to enhanced expressions of an inducible type of NO synthase mRNA and proteins. Intracellular reactive oxygen species (ROS) were exclusively generated in RAW 264.7 cells stimulated with D-GalN and LPS. Scavenging of intracellular ROS abrogated the augmentation of NO production. It was therefore suggested that D-GalN might augment LPS-induced NO production through the generation of intracellular ROS.
研究了D-半乳糖胺（D-GalN）对脂多糖（LPS）刺激的RAW 264.7巨噬细胞中一氧化氮（NO）产生的影响。D-GalN增强了LPS刺激的RAW 264.7细胞中NO的产生，但不增强肿瘤坏死因子（TNF）-α的产生。D-GalN预处理增强了NO的产生，而后处理则没有。D-GalN增强了用TNF-α和干扰素-γ刺激的RAW 264.7细胞中NO的产生。D-GalN增强LPS诱导的NO产生是由于诱导型NO合酶mRNA和蛋白质的表达增强。细胞内活性氧（ROS）仅在D-GalN和LPS刺激的RAW 264.7细胞中产生。清除细胞内ROS消除了NO产生的增强。因此，提示D-GalN可能通过产生细胞内ROS来增强LPS诱导的NO产生。
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