Excessive inflammatory response caused by infiltration of a large number of neutrophils is one of the important features of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Lipoxin A4 (LXA4) is an important endogenous mediator in the process of inflammation resolution, which has a strong role in promoting inflammation resolution. In this study, we examined the impact of LXA4 on the pulmonary inflammatory response and the neutrophil function in ARDS rats. Our results indicated that exogenous administration of LXA4 could reduce the degree of lung injury in ARDS rats and inhibit the release of pro-inflammatory factors TNF-α and IL-1β in lung tissue homogenate. However, LXA4 has no lung protective effect on ARDS rats of neutropenia, nor can it inhibit the levels of pro-inflammatory factors TNF-α and IL-1β in lung tissue homogenate. LXA4 can inhibit the production of reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) in peripheral blood neutrophils of ARDS rats. At the same time, LXA4 can promote the phagocytosis of neutrophils in ARDS rats in vitro and can also promote the apoptosis of neutrophils in ARDS rats. In addition, the effect of LXA4 on the function of neutrophils in ARDS rats is mediated by its receptor ALX. LXA4 can inhibit the release of NE and MPO from neutrophils, thereby reducing the production of NETs. In summary, these findings indicate that LXA4 has a protective effect on LPS-induced ARDS rats by affecting the function of neutrophils.

大量中性粒细胞浸润引起的过度炎症反应是急性肺损伤（ALI）/急性呼吸窘迫综合征（ARDS）的重要特征之一。脂氧素A4（LXA4）是炎症消退过程中重要的内源性介质，具有很强的促进炎症消退的作用。在这项研究中，我们检查了 LXA4 对 ARDS 大鼠肺部炎症反应和中性粒细胞功能的影响。我们的研究结果表明，外源给予LXA4可以减轻ARDS大鼠的肺损伤程度，并抑制肺组织匀浆中促炎因子TNF-α和IL-1β的释放。但LXA4对中性粒细胞减少的ARDS大鼠没有肺保护作用，也不能抑制肺组织匀浆中促炎因子TNF-α和IL-1β的水平。LXA4 可以抑制 ARDS 大鼠外周血中性粒细胞中活性氧 (ROS) 和中性粒细胞胞外陷阱 (NETs) 的产生。同时LXA4可促进ARDS大鼠中性粒细胞的吞噬作用在体外也能促进ARDS大鼠中性粒细胞的凋亡。此外，LXA4对ARDS大鼠中性粒细胞功能的影响是由其受体ALX介导的。LXA4 可以抑制中性粒细胞释放 NE 和 MPO，从而减少 NETs 的产生。总之，这些发现表明LXA4通过影响中性粒细胞的功能对LPS诱导的ARDS大鼠具有保护作用。