Milligan S A, Owens M W, Grisham M B
Department of Medicine, Veterans Affairs Medical Center, Shreveport, Louisiana 71101, USA.
Am J Physiol. 1996 Jul;271(1 Pt 1):L114-20. doi: 10.1152/ajplung.1996.271.1.L114.
The inducible isoform of nitric oxide synthase (iNOS) is induced upon stimulation of cells with cytokines and lipopolysaccharide (LPS). Stimulation of rat pleural mesothelial cells with combinations of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), and LPS induced the synthesis of nitric oxide as measured by the oxidation products nitrite (NO2-) and nitrate (NO3-). Addition of 25-50 microM H2O2 to the cytokines significantly augmented the synthesis of NO2- and NO3-. Stimulation with IL-1 beta and TNF-alpha plus H2O2 or IL-1 beta and LPS plus H2O2 increased the synthesis of NO2- and NO3- by 3.8- and 3.5-fold, respectively. These effects were inhibited by NG-nitro-L-arginine methyl ester and cycloheximide as well as by catalase. Immunoblotting demonstrated that H2O2 augmented cytokine-induced synthesis of iNOS protein. These effects were inhibited by certain antioxidants and metal chelators, suggesting that the hydroxyl radical may mediate the oxidant-induced effect. Northern blotting demonstrated that H2O2 greatly augmented steady-state levels of iNOS mRNA, suggesting that H2O2 acted in part at the transcriptional level.
一氧化氮合酶(iNOS)的可诱导同工型在细胞受到细胞因子和脂多糖(LPS)刺激时被诱导。用白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、干扰素-γ(IFN-γ)和LPS的组合刺激大鼠胸膜间皮细胞,通过氧化产物亚硝酸盐(NO2-)和硝酸盐(NO3-)来测量,可诱导一氧化氮的合成。向细胞因子中添加25 - 50微摩尔的过氧化氢(H2O2)可显著增强NO2-和NO3-的合成。用IL-1β和TNF-α加H2O2或IL-1β和LPS加H2O2刺激分别使NO2-和NO3-的合成增加了3.8倍和3.5倍。这些作用被NG-硝基-L-精氨酸甲酯、放线菌酮以及过氧化氢酶所抑制。免疫印迹表明,H2O2增强了细胞因子诱导的iNOS蛋白合成。这些作用被某些抗氧化剂和金属螯合剂所抑制,表明羟基自由基可能介导了氧化剂诱导的效应。Northern印迹表明,H2O2极大地提高了iNOS mRNA的稳态水平,表明H2O2部分作用于转录水平。