Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2000
Protective involvement of nitric oxide in the liver injury induced by delayed-type hypersensitivity to picryl chloride.
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Cao J, Xu Q, Koda A
Аннотация
OBJECTIVE AND DESIGN: To investigate the role of nitric oxide (NO) in the liver injury induced by delayed-type hypersensitivity to picryl chloride (PCl-DTH).
MATERIALS AND METHODS: Liver injury was induced in mice by PCl-DTH. NO production was examined using the Griess reagent. Isolated hepatocytes (HC) and nonparenchymal cells (NPC) were used.
RESULTS: NO production in both serum and liver tissue reached a peak at 36 h after the elicitation of liver injury. The in vitro NO production was only observed by NPC or HC isolated at 24 h after the injury. Co-stimulation of IFN-gamma and TNF-alpha significantly triggered the HC and NPC isolated at 0 h to produce NO. As NO synthase inhibitors, Nomega-Nitro-L-Arginine exacerbated the liver injury in mice and NG-Monomethyl-L-Arginine enhanced the hepatotoxicity of IFN-gamma and TNF-alpha in vitro. In contrast, NO producer, S-nitroso-N-acetylpenicillamine dose-dependently inhibited the hepatotoxicity of NPC.
CONCLUSIONS: NO may be produced by HC and NPC under the co-stimulation of IFN-gamma and TNF-alpha, and may play an important role for alleviating the liver injury.
MATERIALS AND METHODS: Liver injury was induced in mice by PCl-DTH. NO production was examined using the Griess reagent. Isolated hepatocytes (HC) and nonparenchymal cells (NPC) were used.
RESULTS: NO production in both serum and liver tissue reached a peak at 36 h after the elicitation of liver injury. The in vitro NO production was only observed by NPC or HC isolated at 24 h after the injury. Co-stimulation of IFN-gamma and TNF-alpha significantly triggered the HC and NPC isolated at 0 h to produce NO. As NO synthase inhibitors, Nomega-Nitro-L-Arginine exacerbated the liver injury in mice and NG-Monomethyl-L-Arginine enhanced the hepatotoxicity of IFN-gamma and TNF-alpha in vitro. In contrast, NO producer, S-nitroso-N-acetylpenicillamine dose-dependently inhibited the hepatotoxicity of NPC.
CONCLUSIONS: NO may be produced by HC and NPC under the co-stimulation of IFN-gamma and TNF-alpha, and may play an important role for alleviating the liver injury.
Предметные рубрики MeSH
AnimalsCells, CulturedChemical and Drug Induced Liver InjuryEnzyme InhibitorsFemaleHepatocytesHypersensitivity, DelayedInterferon-gammaLiverLiver DiseasesMaleMiceMice, Inbred BALB CNitric OxideNitric Oxide DonorsPenicillaminePicryl ChlorideTime FactorsTumor Necrosis Factor-alphaomega-N-Methylarginine