小鼠腹腔巨噬细胞诱生性一氧化氮的诱导合成  

Inducible NO Synthesis in Activated Murine Macrophages

作　　者：牛宇欣[1] 李慧珠[1] 郑思华[1] 王新荣[1] 

机构地区：[1]首都医科大学分子生物学系

出　　处：《实验动物科学与管理》1999年第1期34-36,共3页Laboratory Animal Science & Administration

摘　　要：通过体外分离培养和体内注射ＩＦＮ－γ，研究了巨噬细胞内一氧化氮（ｎｉｔｒｉｃｏｘｉｄｅ，ＮＯ）的诱导合成。体外培养条件下，ＩＦＮ－γ能够诱导小鼠腹腔巨噬细胞合成一氧化氮，与对照组相比有显著差异（Ｐ＜００１）。巨噬细胞内一氧化氮的诱导合成水平同ＩＦＮ－γ的剂量有关。ＴＮＦ－α能够显著增强ＩＦＮ－γ的诱导合成ＮＯ作用。ＩＦＮ－γ在体内可以增强巨噬细胞的一氧化氮合成能力。研究表明，诱导巨噬细胞合成一氧化氮是一种非特异性免疫反应，ＩＦＮ－γ诱导免疫细胞通过Ｌ－精氨酸途径合成一氧化氮有可能是宿主抵抗感染的重要机制。Using BALB/c mice as model animal, we studied inducible nitric oxide (NO) synthesis in activated murine macrophages. Activated murine macrophage can synthessis NO through an L arginine pathway which is toxic to sorts of pathogen and tumor cell. The synthesis of NO by IFN γ activated murine macrophages was investigated. Shortly after stimulated with IFN γ directly in vitro, macrophages synthesized and released NO.The amount of released NO is related with the dosage of stimulating IFN γ. TNF α significantly enhanced macrophages NO synthesis. Macrophages, separated from BALB/c mice that had been injected with 10000μ IFN γ,released large amount of NO, which is remarkably different with control group mice ( P <0 01). These results suggested that synthesis inducible is a kind of nonspecific response to stimulus, which played an important role in immunological response against infection.

关 键 词：一氧化氮 巨噬细胞 非特异性免疫 IFN-Γ TNF-Α 

分 类 号：R392[医药卫生—免疫学] R－332[医药卫生—基础医学]