Sherman M P, Aeberhard E E, Wong V Z, Griscavage J M, Ignarro L J
Department of Pediatrics, UCLA School of Medicine 90024.
Biochem Biophys Res Commun. 1993 Mar 31;191(3):1301-8. doi: 10.1006/bbrc.1993.1359.
Since nuclear factor kappa B (NF-kappa B) is activated during many inflammatory conditions, we assessed its role in expression of the L-arginine-nitric oxide pathway by rat alveolar macrophages. Pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-kappa B activation, was added to cultured macrophages stimulated with lipopolysaccharide (LPS) and interferon-gamma (IFN gamma). Inducible nitric oxide synthase (iNOS) activity was determined by measuring the stable nitrogen oxide end products of L-arginine oxidation: nitrite (NO2-) and nitrate (NO3-). Ten, 25 and 50 microM PDTC progressively inhibited iNOS activity by macrophages. When 50 microM PDTC was added 2 h before LPS + IFN gamma, L-arginine oxidation by macrophages was inhibited by > 99%; L-arginine oxidation was reduced by 70% if 50 microM PDTC and the stimuli were introduced together; NO2- and NO3- were not decreased significantly if 50 microM PDTC was added 6 h after LPS + IFN gamma. Cycloheximide added along with LPS + IFN gamma totally inhibits iNOS activity, while cycloheximide added 6 h after LPS + IFN gamma did not reduce NO2- and NO3- in tissue culture supernatants. These findings suggest iNOS activity in macrophages treated with LPS + IFN gamma requires NF-kappa B activation.
由于核因子κB(NF-κB)在多种炎症状态下被激活,我们评估了其在大鼠肺泡巨噬细胞中对L-精氨酸-一氧化氮途径表达的作用。吡咯烷二硫代氨基甲酸盐(PDTC)是一种NF-κB激活抑制剂,被添加到用脂多糖(LPS)和干扰素-γ(IFNγ)刺激的培养巨噬细胞中。通过测量L-精氨酸氧化的稳定氮氧化物终产物:亚硝酸盐(NO2-)和硝酸盐(NO3-)来测定诱导型一氧化氮合酶(iNOS)的活性。10、25和50微摩尔的PDTC可逐渐抑制巨噬细胞的iNOS活性。当在LPS + IFNγ刺激前2小时添加50微摩尔的PDTC时,巨噬细胞的L-精氨酸氧化被抑制> 99%;如果同时加入50微摩尔的PDTC和刺激物,L-精氨酸氧化减少70%;如果在LPS + IFNγ刺激后6小时添加50微摩尔的PDTC,NO2-和NO3-没有显著降低。与LPS + IFNγ一起添加的放线菌酮完全抑制iNOS活性,而在LPS + IFNγ刺激后6小时添加放线菌酮并没有降低组织培养上清液中的NO2-和NO3-。这些发现表明,用LPS + IFNγ处理的巨噬细胞中的iNOS活性需要NF-κB激活。