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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >MICE LACKING INDUCIBLE NITRIC OXIDE SYNTHASE ARE NOT RESISTANT TO LIPOPOLYSACCHARIDE-INDUCED DEATH
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MICE LACKING INDUCIBLE NITRIC OXIDE SYNTHASE ARE NOT RESISTANT TO LIPOPOLYSACCHARIDE-INDUCED DEATH

机译：小鼠缺乏可诱导的一氧化氮合酶对脂多糖诱导的死亡没有抵抗力

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Nitric oxide produced by cytokine-inducible nitric oxide synthase (iNOS) is thought to be important in the pathogenesis of septic shock. To further our understanding of the role of iNOS in normal biology and in a variety of inflammatory disorders, including septic shock,,ve have used gene targeting to generate a mouse strain that lacks iNOS. Mice lacking iNOS were indistinguishable from mild-type mice in appearance and histology. Upon treatment with lipopolysaccharide and interferon gamma, peritoneal macrophages from the mutant mice did not produce nitric oxide measured as nitrite in the culture medium. In addition, lysates of these cells did not contain iNOS protein by immunoblot analysis or iNOS enzyme activity. In a Northern analysis of total RNA, no iNOS transcript of the correct size was detected. No increases in serum nitrite plus nitrate levels were observed in homozygous mutant mice treated with a lethal dose of lipopolysaccharide, but the mutant mice exhibited no significant survival advantage over wild-type mice, These results show that lack of iNOS activity does not prevent mortality in this murine model for septic shock. [References: 51]
机译：由细胞因子诱导型一氧化氮合酶（iNOS）产生的一氧化氮被认为在败血性休克的发病机理中很重要。为了进一步了解iNOS在正常生物学和各种炎症性疾病（包括败血性休克）中的作用，已经使用基因靶向来产生缺乏iNOS的小鼠品系。缺乏iNOS的小鼠在外观和组织学上与轻度小鼠没有区别。用脂多糖和干扰素γ治疗后，突变小鼠的腹膜巨噬细胞在培养基中未产生亚硝酸盐形式的一氧化氮。另外，通过免疫印迹分析或iNOS酶活性，这些细胞的裂解物不包含iNOS蛋白。在总RNA的Northern分析中，未检测到正确大小的iNOS转录本。在用致死剂量的脂多糖处理的纯合突变小鼠中，没有观察到血清亚硝酸盐和硝酸盐水平的增加，但是与野生型小鼠相比，突变小鼠没有明显的生存优势。这些结果表明，缺乏iNOS活性并不能防止死亡。这种鼠类感染性休克模型。 [参考：51]

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