Excessive in ammatory response caused by in ltration 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 in ammation resolution, which has a strong role in promoting in ammation resolution. In this study, we examined the impact of LXA4 on the pulmonary in mmatory response and the neutrophil function in a rat model of ARDS. Our results indicated that Exogenous administration of LXA4 could reduce the degree of lung injury in ARDS rats and inhibit the release of pro-in ammatory factors TNF-α and IL-1β in lung tissue homogenate. However, LXA4 has no lung protective effect on ARDS rats with neutrophil depletion in rats, nor can it inhibit the levels of pro-in ammatory factors TNF-α and IL-1β in lung tissue homogenate. LXA4 can inhibit the production of reactive oxygen species (ROS) and 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 and reduce neutrophil NETosis. In addition, the effect of LXA4 on the function of peripheral blood neutrophils in ARDS rats is mediated by its receptor ALX. LXA4 can inhibit the release of NE and MPO from neutrophils, thereby inhibiting the production of NETs, and the effect of LXA4 can be comparable to NEi and MPO inhibitors. In summary, these ndings indicate that LXA4 has a protective effect on LPS-induced ARDS rats by affecting the function of neutrophils.
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