C3a-induced lysosomal enzyme secretion from human neutrophils: lack of inhibition by f met-leu-phe antagonists and inhibition by arachidonic acid antagonists.
C3a-induced lysosomal enzyme secretion from human neutrophils: lack of inhibition by f met-leu-phe antagonists and inhibition by arachidonic acid antagonists.
复制标题
C3a 诱导的人中性粒细胞分泌溶酶体酶：缺乏 f met-leu-phe 拮抗剂的抑制作用和花生四烯酸拮抗剂的抑制作用。
DOI：
10.1159/000233023
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Ward,PA
中科院分区：
文献类型：
--
作者：
Showell,HJ;Glovsky,MM;Ward,PA
C3a诱导的人外周中性粒细胞以非细胞溶解的、剂量依赖的(10-100μg/ml)过程分泌溶酶体酶。当中性粒细胞暴露于C3a和细胞松弛素B时，初级颗粒成分和次级颗粒成分都被释放，然而，C3a单独诱导溶菌酶的释放是有限的。中性粒细胞上甲酰肽受体的竞争性拮抗剂t BOC(Phe-leu)2-Phe不能阻断C3a诱导的释放。花生四烯酸拮抗剂去甲二氢愈创木酸和槲皮素对C3a+细胞松弛素B诱导的溶菌酶释放有剂量依赖性的抑制作用，但对C3a诱导的溶菌酶释放无明显影响。高浓度(~gt；10~(-5)M)的吲哚美辛也有类似的抑制作用。
C3a-induced lysosomal enzyme secretion from human peripheral neutrophils in a noncytolytic, dose-dependent (10–100 μg/ml) process. Release of both primary and secondary granule constituents occurred when neutrophils were exposed to C3a plus cytochalasin B, however, C3a alone induced limited release of lysozyme. A competitive antagonist of the formyl-peptide receptor on neutrophils, t boc (phe-leu)2-phe, did not block the release induced by C3a. Arachidonic acid antagonists, nordihydroguaiaretic acid and quercetin caused dose-dependent inhibition of release induced by C3a plus cytochalasin B, however, lysozyme release induced by C3a in the absence of cytochalasin B was minimally affected. Indomethacin at high concentration (> 10––5M) had similar inhibitory effects.