应用钙离子通道阻断剂nifedipine和verapamil以及胞内钙离子拮抗剂nicardipilie和ruthenium red,观察了胞内钙离子在Mφ活化杀伤肿瘤细胞的重要性。nifedipine和verapamil不抑制而强烈的增强MAF诱导的Mφ活化,nicardipine和ruthenium red均抑制MAF和钙离子载体A_(23187)诱导的Mφ活化,LPS活化Mφ的作用同样受到抑制。这些结果提示,胞外钙离子可能不参与MAF诱导的Mφ活化,MAF、A_(23187)、LPS活化Mφ的作用是胞内钙离子依赖的。 The importance of intracellular Ca2 + in Mφ-activated killing of tumor cells was observed by using calcium channel blockers nifedipine and verapamil as well as nicardipilie and ruthenium red, an intracellular calcium antagonist. Nifedipine and verapamil did not inhibit but strongly enhanced MAF-induced Mφ activation. Both nicardipine and ruthenium red inhibited Mφ activation induced by MAF and calcium ionophore A_ (23187), and LPS-activated Mφ was also inhibited. These results suggest that extracellular Ca2 + may not be involved in MAF-induced Mφ activation. The effect of MAF, A_ (23187) and LPS activation on Mφ is intracellular Ca2 + dependent.