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一氧化氮是活化的巨噬细胞（Ｍ）在体外杀溶组织内阿米巴滋养体的主要效应分子。本文试图探讨肿瘤坏死因子－α（ＴＮＦ－α）所诱导的Ｍ体外杀伤溶组织内阿米巴滋养体的作用是否与其ＮＯ合成有关。结果表明：（１）ＴＮＦ－α本身不能直接诱导Ｍ产生ＮＯ以杀伤阿米巴，但若与γ－干扰素联合应用，则Ｍ杀伤阿米巴的效力及ＮＯ产量的增加呈显著的线性相关。ＴＮＦ－α抗血清和ＮＯ合成酶抑制剂，一甲基精氨酸（Ｌ－ＮＭＭＡ）可抑制其协同作用。（２）脂多糖（ＬＰＳ）和γ－干扰素共同活化的Ｍ产生的ＴＮＦ－α和ＮＯ的量呈显著的线性相关。ＴＮＦ－α抗血清抑制ＴＮＦ－α和ＮＯ及杀伤阿米巴效力分别为９３％，５３％和８６％，而Ｌ－ＮＭＭＡ虽降低了ＮＯ产量至７４％和杀伤阿米巴效力到８３％，却不影响ＴＮＦ－α的分泌。（３）同样，ＴＮＦ－α也能够与ＬＰＳ共同活化Ｍ产生ＮＯ杀伤阿米巴。这些结果证明ＴＮＦ－α所诱导的Ｍ体外杀伤阿米巴作用与ＮＯ合成途径有关。
Nitric oxide is the main effector molecule that activates macrophages (M) to kill dissolved amebic trophozoites in vitro. This article attempts to investigate whether the effect of M-induced killing of Entamoeba histolytica trophozoites by tumor necrosis factor-α (TNF-α) is related to NO synthesis. The results showed that: (1) TNF-α itself can not directly induce M to produce NO to kill amoeba, but if combined with γ-interferon, the efficacy of M to kill amoeba and the increase of NO production are significantly linearly related . TNF-α antiserum and NO synthase inhibitor, monomethylarginine (L-NMMA) can inhibit its synergistic effect. (2) The amount of TNF-α and NO produced by M co-activated by lipopolysaccharide (LPS) and γ-interferon showed a significant linear correlation. The TNF-α antiserum had 93%, 53%, and 86% inhibition of TNF-α and NO, respectively, while L-NMMA reduced NO production to 74% and killing amoeba efficacy to 83%. Does not affect the secretion of TNF-α. (3) Similarly, TNF-α can also cooperate with LPS to activate M to produce NO to kill amoeba. These results demonstrate that TNF-α-induced killing of amoeba in vitro is associated with the NO synthesis pathway.