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豚鼠嗜酸性粒细胞产生超氧化物的细胞机制及其与颗粒过氧化物酶释放的解离研究。

Studies of cellular mechanisms for the generation of superoxide by guinea-pig eosinophils and its dissociation from granule peroxidase release.

作者信息

Shute J K, Rimmer S J, Akerman C L, Church M K, Holgate S T

机构信息

Immunopharmacology Group, Southampton General Hospital, Hampshire, U.K.

出版信息

Biochem Pharmacol. 1990 Nov 1;40(9):2013-21. doi: 10.1016/0006-2952(90)90231-9.

Abstract

Guniea-pig peritoneal eosinophils generated superoxide anions in response to opsonized zymosan, platelet activating factor, sodium fluoride, digitonin, phorbol ester and calcium ionophore, but were refractory to fMLP. These agonists did not stimulate release of eosinophil peroxidase. The phospholipase inhibitor, mepacrine, and the protein kinase inhibitor, trifluoperazine, were effective inhibitors of superoxide production. Activators of protein kinase C, such as exogenously added phorbol ester and endogenously derived diacylglycerol, stimulate superoxide production, which is therefore proposed to be via pathways dependent on phospholipase and protein kinase activity.

摘要

豚鼠腹腔嗜酸性粒细胞在受到调理酵母聚糖、血小板活化因子、氟化钠、洋地黄皂苷、佛波酯和钙离子载体刺激时会产生超氧阴离子,但对甲酰甲硫氨酸-亮氨酸-苯丙氨酸(fMLP)无反应。这些激动剂不会刺激嗜酸性粒细胞过氧化物酶的释放。磷脂酶抑制剂米帕林和蛋白激酶抑制剂三氟拉嗪是超氧阴离子产生的有效抑制剂。蛋白激酶C的激活剂,如外源性添加的佛波酯和内源性产生的二酰甘油,会刺激超氧阴离子的产生,因此推测这是通过依赖磷脂酶和蛋白激酶活性的途径实现的。

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