脂氧素（lipoxins, LXs）是一种具有抗炎、调节免疫反应、促进细胞损伤修复的内源性脂质介质，被称为炎症反应的“刹车信号”。研究表明，LXs及阿司匹林诱生型脂氧素（aspirin-triggered lipoxin A4, ATL）在调控炎症通路的同时，能通过多种途径促进小胶质细胞和巨噬细胞吞噬凋亡碎片、坏死细胞，发挥促炎症消退、稳定内环境的作用。文章综述相关文献，以了解LXs对吞噬功能作用的最新进展，其机制主要可分为4种： ① 改变细胞极性，重组细胞结构； ② 上调吞噬受体； ③ 激活M2型吞噬细胞； ④ 抑制吞噬细胞凋亡。小胶质细胞及其吞噬功能在多种脑相关疾病中发挥重要作用，研究LXs对吞噬功能的影响也许能为相关脑病的治疗提供思路。
Lipoxins (LXs) are endogenous lipid mediators that play a role on anti-inflammatory action, regulating immune response, and repairing damaged cells. It was also known as "the brake signal" of inflammatory response. Researches revealed that LXs and aspirin-triggered lipoxin A4 (ATL) promote the macrophage cells and microglia cell phagocytose cell debris and apoptotic cells by different ways while it regulates anti-inflammation effect and stabilize internal milieu. We reviewed the research progresses in the study of LXs and phagocytosis and summarized their roles as four mechanisms: ① Changing cell polarity and rebuild cellular structure. ② Up-regulation of specific scavenger receptors. ③ Activating M2 phagocytes. ④ Inhibition the apoptosis of phagocytes. Microglia and its phagocytosis function play vital roles in brain diseases, thus studying LXs may provide new therapeutic strategies.
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