Open AccessThe enhancing action of d ‐galactosamine on lipopolysaccharide‐induced nitric oxide production in RAW 264.7 macrophage cells
Author(s) -
Morikawa Akiko,
Koide Naoki,
Sugiyama Tsuyoshi,
Mu Mya Mya,
Hassan Ferdaus,
Islam Shamima,
Ito Hiroyasu,
Mori Isamu,
Yoshida Tomoaki,
Yokochi Takashi
Publication year - 2004
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1016/j.femsim.2004.03.008
Subject(s) - nitric oxide , lipopolysaccharide , intracellular , macrophage , tumor necrosis factor alpha , galactosamine , reactive oxygen species , biology , nitric oxide synthase , biochemistry , downregulation and upregulation , immunology , endocrinology , in vitro , glucosamine , gene
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)‐α 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‐α and interferon‐γ. 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.