目的探讨褪黑素（ＭＴ）抑制一氧化氮生成与保护免疫性肝损伤的关系。方法用短小棒状杆菌和脂多糖诱导小鼠免疫性肝损伤模型；分离、培养肝细胞和腹腔巨噬细胞；检测一氧化氮（ＮＯ）、丙氨酸氨基转换酶（ＡＬＴ）、丙二醛（ＭＤＡ）和谷胱甘肽过氧化酶（ＧＳＨｐｘ）变化。结果ＭＴ在０１～１０ｍｇ·ｋｇ－１·ｄ－１浓度范围内，明显降低小鼠免疫性肝损伤中ＭＬＴ和ＭＤＡ水平，部分恢复ＧＳＨｐｘ活性（Ｐ＜００５～００１），同时血浆ＮＯ水平下降（Ｐ＜００５）。左旋单甲基精氨酸则在显著降低血浆ＮＯ水平（Ｐ＜００１）同时，肝损伤征象加重。体外用ＭＴ对肝细胞和巨噬细胞无明显影响。结论褪黑素抑制体内ＮＯ过度生成，有利于保护免疫性肝损伤。 Objective To investigate the relationship between melatonin (MT) inhibition of nitric oxide production and protection of immune liver injury. Methods Immunological liver injury model was induced in mice with Corynebacterium parvum and lipopolysaccharide. Hepatocytes and peritoneal macrophages were isolated and cultured. Nitric oxide (NO), alanine aminotransferase (ALT) and malondialdehyde MDA) and glutathione peroxidase (GSH-px) changes. Results In the range of 01-10 mg · kg-1 · d-1, MT significantly decreased the level of MLT and MDA in mice with autoimmune liver injury and partially restored the activity of GSHpx (P <005 ~ 0  01), while plasma NO levels decreased (P <0  05). L-Monomethyl arginine significantly reduced plasma NO levels (P <001), while signs of liver injury worsened. In vitro MT had no significant effect on hepatocytes and macrophages. Conclusion Melatonin can inhibit the excessive production of nitric oxide and protect the immune liver injury.