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Formation of endogenous "antiinflammatory" lipid mediators by transcellular biosynthesis. Lipoxins and aspirin-triggered lipoxins inhibit neutrophil recruitment and vascular permeability.

作者信息

Serhan C N, Takano T, Chiang N, Gronert K, Clish C B

机构信息

Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesia, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

出版信息

Am J Respir Crit Care Med. 2000 Feb;161(2 Pt 2):S95-S101. doi: 10.1164/ajrccm.161.supplement_1.ltta-19.

DOI:10.1164/ajrccm.161.supplement_1.ltta-19
PMID:10673235
Abstract
摘要

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Formation of endogenous "antiinflammatory" lipid mediators by transcellular biosynthesis. Lipoxins and aspirin-triggered lipoxins inhibit neutrophil recruitment and vascular permeability.通过跨细胞生物合成形成内源性“抗炎”脂质介质。脂氧素和阿司匹林触发的脂氧素可抑制中性粒细胞募集和血管通透性。
Am J Respir Crit Care Med. 2000 Feb;161(2 Pt 2):S95-S101. doi: 10.1164/ajrccm.161.supplement_1.ltta-19.
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