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目的:研究肺巨噬细胞(Mφ)内诱导型一氧化氮合酶(iNOS)及其产物一氧化氮(NO)在抗肿瘤免疫中的作用。方法:取小鼠肺泡灌洗液,用体外细胞培养技术,并加入不同剂量的干扰素γ(INFγ)制成肺Mφ悬液,与肿瘤P815细胞培养后测定NOS活性及NO含量;同时测定加特异性NOS抑制剂NG单甲基左旋精氨酸(L-NMMA)和不加L-NMMA的肺Mφ肿瘤杀伤活性的抑制率。结果:不同剂量INFγ与活化的肺Mφ共同培养后,培养液中NO含量随着INFγ剂量的增加而升高,且呈明显的剂量依赖关系(r=0.985,t=19.89,P<0.01);同时肺MφiNOS的活性也随着INFγ剂量的增加而升高,两者呈显著正相关(r=0.990,t=19.78,P<0.01);预先加入L-NMMA的活化肺Mφ与P815细胞培养液中,NO含量减低(P<0.05),对P815抑制率明显降低(P<0.05)。结论:活化的肺Mφ中由iNOS催化产生的NO是杀伤肿瘤细胞的一个重要效应分子。
Objective: To investigate the role of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) in lung macrophages (Mφ) in antitumor immunity. METHODS: Mice were treated with bronchoalveolar lavage fluid and cultured in vitro with different doses of interferon gamma (INFγ) to make lung Mφ suspension. The activity of NOS and NO were measured after incubation with tumor P815 cells. Specific NOS inhibitor NG monomethyl L-arginine (L-NMMA) and L-NMMA-free lung Mφ tumor-killing activity inhibition rate. Results: After different doses of INFγ were co-cultured with activated lung Mφ, the NO content in culture medium increased with the increase of INFγ dose, and showed a significant dose-dependent relationship (r=0.985, t=19.89, P<0.01); At the same time, the activity of lung MφiNOS also increased with the increase of INFγ dose, there was a significant positive correlation between the two (r=0.990, t=19.78, P<0.01); activated lung Mφ and P815 cell culture fluid pre-incorporated with L-NMMA In the study, the content of NO was decreased (P<0.05), and the inhibition rate of P815 was significantly decreased (P<0.05). CONCLUSION: Nitric oxide catalyzed by iNOS in activated lung Mφ is an important effector molecule that kills tumor cells.