Showell H J, Glovsky M M, Ward P A
Int Arch Allergy Appl Immunol. 1982;67(3):227-32. doi: 10.1159/000233023.
C3a-induced lysosomal enzyme secretion from human peripheral neutrophils in a noncytolytic, dose-dependent (10-100 microgram/ml) process. Release of both primary and secondary granule constituents occurred when neutrophils were exposed to C3a plus cytochalasin B, however, C3 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 (greater than 10(-5) M) had similar inhibitory effects.
C3a 以非细胞溶解的、剂量依赖性（10 - 100微克/毫升）过程诱导人外周血中性粒细胞溶酶体酶分泌。当中性粒细胞暴露于C3a加细胞松弛素B时，初级和次级颗粒成分均会释放，然而，单独的C3仅诱导有限的溶菌酶释放。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加细胞松弛素B诱导的释放产生剂量依赖性抑制，然而，在不存在细胞松弛素B的情况下，C3a诱导的溶菌酶释放受到的影响最小。高浓度（大于10^(-5) M）的吲哚美辛具有类似的抑制作用。
