Hernández-Godoy J, Planelles D, Balsalobre B, González-Molina A
Unidad de Inmunología Experimental, Hospital La Fe, Valeneia, Spain.
Int J Clin Lab Res. 1996;26(3):185-91. doi: 10.1007/BF02592980.
The purpose of this study was to analyze the effects of nordihydroguaiaretic acid, an inhibitor of the lipoxygenase pathway of arachidonic acid, on antibody-dependent cellular cytotoxicity. Antibody-dependent cellular cytotoxicity mediated by murine spleen cells was significantly inhibited by concentrations of nordihydroguaiaretic acid from 10(-5) to 10(-4) M (1C50 = 2 x 10(-5) M). The inhibitory effect of nordihydroguaiaretic acid was also observed on antibody-dependent cellular cytotoxicity mediated by macrophage-depleted spleen cells as well as isolated macrophages. Nordihydroguaiaretic acid was highly effective when added at the beginning of the assay and was always present throughout the assay, but failed to inhibit the binding of effector and target cells. The inhibition produced by nordihydroguaiaretic acid could not be reversed by leukotriene B4, a 5-lipoxygenase product. These results suggest that arachidonic acid metabolites other than leukotriene B4 are released by different populations of spleen cells to positively regulate important events in the postbinding phase of murine antibody-dependent cellular cytotoxicity.
本研究的目的是分析花生四烯酸脂氧合酶途径抑制剂去甲二氢愈创木酸对抗体依赖性细胞毒性的影响。浓度为10(-5)至10(-4)M的去甲二氢愈创木酸可显著抑制小鼠脾细胞介导的抗体依赖性细胞毒性（半数抑制浓度=2×10(-5)M）。在巨噬细胞耗尽的脾细胞以及分离的巨噬细胞介导的抗体依赖性细胞毒性中，也观察到了去甲二氢愈创木酸的抑制作用。在试验开始时添加去甲二氢愈创木酸非常有效，并且在整个试验过程中一直存在，但它未能抑制效应细胞与靶细胞的结合。白三烯B4（一种5-脂氧合酶产物）不能逆转去甲二氢愈创木酸产生的抑制作用。这些结果表明，除白三烯B4外的花生四烯酸代谢产物由不同的脾细胞群体释放，以正向调节小鼠抗体依赖性细胞毒性结合后阶段的重要事件。
