Parturition is the physiological process of newborn birth; more and more evidences show that parturition is closely related to the occurrence and resolution of inflammation. However, the inflammatory media and the mechanism are not very clear during parturition. Here, we investigate the inflammatory event during human parturition and in mouse model. We found that the pro-inflammatory cytokines (IL-6, IL-8, and IL-1 beta) and cells (neutrophil and macrophage) are decreased in pregnant women in labor and in mouse labor model. Mechanistically, increased stress stimulates the high-level adrenaline production in labor. Then, adrenaline upregulates the expression of 12/15-LOX (lipoxygenase) to produce more lipoxin A4 (LXA4), which is an inflammation inhibitor. Thus, LXA4 promotes the elimination of inflammation during labor to protect the body from excessive inflammatory damages. In addition, using BOC-2, the inhibitor of LXA4 receptor could reboot the pro-inflammatory cytokines. Our study indicates that LXA4 is induced by adrenaline in labor and appropriate interference of this pathway may be a potential strategy to regulate the inflammatory process in parturition.