一氧化氮与活化的小鼠腹腔巨噬细胞细胞毒作用关系的研究  

Studies on the Relationship between Nitric Oxide and the Cytotoxicity Mediated by Activated Murine Peritoneal Macrophages

作　　者：包建军[1] 邢嵘[2] 于丽华[2] 钱振超[2] 

机构地区：[1]日本前桥市群马大学医学部药理学教室 [2]大连医科大学病理生理学教研室,大连116027

出　　处：《上海免疫学杂志》1998年第5期283-286,共4页Shanghai Journal of Immunology

摘　　要：本文选用Raji和K562两种细胞株作靶细胞,以LPS和IFN-γ作为巨噬细胞(MΦ)的激活剂,研究了一氧化氮(NO)在活化的小鼠腹腔巨噬细胞(PEMΦ)细胞毒中的作用以及靶细胞对MΦ合成NO的影响.结果表明,PEMΦ被激活后,合成NO量大为增加,并对Raji和K562两种靶细胞表现出很高的细胞毒效应;加入NO合酶抑制剂L-NMMA,PEMΦ对Raji的杀伤作用受到显著抑制,而对K562的细胞毒作用则不受影响.此外,在实验条件下,Raji细胞的存在可促进PEMΦ产生NO,而K562细胞则有削弱PEMΦ合成NO的倾向.In this paper, we further investigated the role of NO in the cytotoxicity of activated murine peritoneal macrophages (PEMφ) and the effect of different tumor target cells on NO production by macrophages. Two human lymphoma/leukemic cell lines , Raji and K562, were selected as target cells. The results showed that when activated by IFN-γ plus LPS, PEMφs were found to produce large amount of NO and exhibit strong cytotoxicity against both Raji and K562 cells. While L-NMMA, a specific inhibitor of nitric oxide synthase (NOS), showing marked inhibition of NO production by activated PEMφ, could only greatly decrease the tumoricidal activity of PEM φ against Raji cells,and not against K562 cells. Moreover under certain conditions, the presence of Raji cells did enhance NO production by activated PEMφ, while the presence of K562 cells showed a contrary way in affecting NO production.

关 键 词：一氧化氮 巨噬细胞 细胞毒 抗肿瘤 

分 类 号：R392.12[医药卫生—免疫学] R73－36[医药卫生—基础医学]