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花生四烯酸的释放：补体晚期成分的一项新功能。

Release of arachidonic acid: a new function of the late complement components.

作者信息

Betz M, Hänsch G M

出版信息

Immunobiology. 1984 May;166(4-5):473-83. doi: 10.1016/S0171-2985(84)80024-8.

DOI:10.1016/S0171-2985(84)80024-8
PMID:6434404
Abstract

Incubation of Ehrlich-ascites cells with sublytic complement doses results in degradation of membrane phospholipids and release of arachidonic acid. Phospholipase A2 blockers inhibit arachidonic acid release indicating a phospholipase dependent cleavage of the phospholipids. Phospholipase A2 is apparently activated during complement-membrane interaction, representing a new reactivity of the late complement components.

摘要

用亚溶细胞剂量的补体孵育艾氏腹水细胞会导致膜磷脂降解并释放花生四烯酸。磷脂酶A2阻滞剂可抑制花生四烯酸释放，表明磷脂的裂解依赖于磷脂酶。磷脂酶A2显然在补体与膜相互作用期间被激活，这代表了补体晚期成分的一种新反应性。

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1
Release of arachidonic acid: a new function of the late complement components.花生四烯酸的释放：补体晚期成分的一项新功能。
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引用本文的文献

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Complement profiles in human skin lymph during the course of irritant contact dermatitis.刺激性接触性皮炎病程中人体皮肤淋巴管内的补体谱。
Arch Dermatol Res. 1994;286(7):359-63. doi: 10.1007/BF00371793.
2
The recovery of human polymorphonuclear leucocytes from sublytic complement attack is mediated by changes in intracellular free calcium.人多形核白细胞从亚溶细胞性补体攻击中的恢复是由细胞内游离钙的变化介导的。
Biochem J. 1985 Oct 1;231(1):205-8. doi: 10.1042/bj2310205.
3
A role for thromboxane in complement-mediated glomerular injury.血栓素在补体介导的肾小球损伤中的作用。
Am J Pathol. 1987 Jul;128(1):45-51.
4
Human rheumatoid synovial cell stimulation by the membrane attack complex and other pore-forming toxins in vitro: the role of calcium in cell activation.膜攻击复合物及其他成孔毒素对人类风湿性滑膜细胞的体外刺激：钙在细胞活化中的作用
Immunology. 1990 Nov;71(3):312-6.
5
Infectious diseases associated with complement deficiencies.与补体缺陷相关的传染病。
Clin Microbiol Rev. 1991 Jul;4(3):359-95. doi: 10.1128/CMR.4.3.359.