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目的：观察一氧化氮和ＩＬ１０对肺泡巨噬细胞炎症反应的调节作用．方法：小鼠肺泡巨噬细胞（ＡＭ）受脂多糖（ＬＰＳ）１０ｍｇ·Ｌ－１刺激同时，加入一氧化氮合酶抑制剂Ｓ硫酸甲基异硫脲（ＳＭＴ）或一氧化氮供体Ｓ亚硝基乙酰青霉胺（ＳＮＡＰ）．ＥＬＩＳＡ法测定上清液中ＴＮＦα、ＩＬ１β、ＩＬ６和ＩＬ１０浓度．结果：ＡＭ受ＬＰＳ刺激后，ＴＮＦα、ＩＬ１β和ＩＬ６释放峰值分别在６、１２和２４小时．ＳＭＴ抑制一氧化氮释放，但促进ＩＬ１β和ＩＬ６释放，对ＴＮＦα无影响．ＳＮＡＰ对ＩＬ１β和ＩＬ６释放有明显的抑制作用，呈剂量依赖效应．重组ＩＬ１０抑制ＴＮＦα、ＩＬ１β和ＩＬ６释放，而ＩＬ１０单克隆抗体促进上述因子释放．结论：内源及外源性一氧化氮和ＩＬ１０均对ＬＰＳ诱导的炎症性细胞因子释放有抑制作用．
Objective: To observe the regulatory effect of nitric oxide and IL10 on the inflammatory response of alveolar macrophages. Methods: The alveolar macrophages (AMs) of mice were stimulated by lipopolysaccharide (LPS) 10 mg · L-1, and the nitric oxide synthase inhibitor S-methyl isothiourea (SMT) or nitric oxide donor S nitroso penicillamine (SNAP). ELISA method to determine the supernatant TNFα, IL 1β, IL 6 and IL 10 concentrations. Results: After stimulated by LPS, the release peak of TNFα, IL1β and IL6 were 6, 12 and 24 hours respectively. SMT inhibit nitric oxide release, but to promote IL 1β and IL 6 release, no effect on TNFα. SNAP IL 1β and IL 6 release significantly inhibited the role of dose-dependent effect. Recombinant IL 10 inhibition of TNFα, IL 1β and IL 6 release, and IL 10 monoclonal antibody to promote the release of these factors. Conclusion: Both endogenous and exogenous nitric oxide and IL-10 inhibit LPS-induced inflammatory cytokine release.