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We examined whether intracellular reactive oxygen and nitrogen intermediates (ROI and RNI) could augment cytokine gene expression.Heparin anticoagulated whole blood and cell lines were stimulated in the presence and absence of antioxidants or an inhibitor of nitric-oxide synthase (NOS) and the suppression of cytokines measured.Dimethylsulfoxide ( Me_2SO)at a concentration of 1% v/v inhibited IL-8 production by 90 % in whole blood stimulated with LPS 1 mg·L~(-1), PHA 10 mg·L~(-1),or immune complexes 250 mg·L~(-1) Transcription of mRNA coding for IL-8 was inhibited by Me_2 SO.The decrease in IL-8 was highly specific, since there was no reduction in viability, or production of TNF, IL-6 or IL-1β. Groα, another member of the C- X- C chemokine family, was also significantly inhibited by Me_2SO[(1.2±0.3) vs (0±0)μg·L~(-1)].Members of the C- C chemokine family were not inhibited by Me_2SO[RANTES: LPS (15±1.6) vs LPS + Me_2SO (19±9) and MIP-
We examined whether intracellular reactive oxygen and nitrogen intermediates (ROI and RNI) could augment cytokine gene expression. Hepatarin anticoagulated whole blood and cell lines were stimulated in the presence and absence of antioxidants or an inhibitor of nitric-oxide synthase (NOS) and the suppression of cytokines measured in a concentration of 1% v / v inhibited IL-8 production by 90% in whole blood stimulated with LPS 1 mg · L -1, PHA 10 mg · L -1 ), or immune complexes 250 mg · L -1 Transcription of mRNA coding for IL-8 was inhibited by Me_2 SO. decrease in IL-8 was highly specific, since there was no reduction in viability, or production of TNF , IL-6 or IL-1β. Groα, another member of the C-X-C chemokine family, was also significantly inhibited by Me_2SO [(1.2 ± 0.3) vs (0 ± 0) μg · L -1] . Members of the C-C chemokine family were not inhibited by Me_2SO [RANTES: LPS (15 ± 1.6) vs LPS + Me_2SO (19 ± 9) and MIP-