一氧化氮是GM_3激活巨噬细胞介导细胞毒的效应分子

NITRIC OXIDE IS THE EFFECTOR MOLECULE OF MACROPHAGEMEDIATED TUMOR CYTOTOXOCITY INDUCED BY GANGLIOSIDE GM3

已报道了神经节苷脂ＧＭ３在体外能激活小鼠腹腔巨噬细胞介导的细胞毒效应（ＭＴＣ），在此基础上发现ＧＭ３又同时可诱导巨噬细胞合成一氧化氮。后者的合成与巨噬细胞的细胞毒效应呈正相关关系（ｒ＝０．９６４，Ｐ＜０．００１）。ＮＯ合酶的抑制剂氨基胍，能显著地减弱ＭＴＣ。上述结果提示，在ＧＭ３激活的ＭＴＣ中。

he authors had reported that ganglioside GM3 could in vitro induce the macrophagemediated tumor cytotoxicity(MTC). In the present study, the authors have further demonstrated that GM3 could induce not only MTC, but also the formation of NO by murine peritoneal Mφs. The MTC and NO inductions are positively correlated(r=0964,P<0001), Aminoguanidine, the inducible nitric oxide synthase selective inhibitor, could abolish the MTC induction. These results suggest that NO is the effector molecule in GM3induced MTC of murine peritoneal Mφs.