Objective: To investigate the effect of lipoxin receptor agonist BML-111 on the NLRP3 inflammasome after traumatic brain injury in rats. Methods: Sixty male Sprague-Dawley rats, weighing 280～340 g, were randomly divided into 4 groups (n = 15): the sham operation group (group Sham), the traumatic brain injury group (group TBI), the BML-111 treatment group (group BML-111), and the BOC-2 treatment group (group BOC-2). The TBI model was prepared by craniocerebral collision, while the rats in group Sham underwent only craniotomy without collision. Acute traumatic brain injury model was prepared in group TBI, BML-111 and BOC-2. The rats in group BOC-2 were intraperitoneally injected with 50 μg/kg of BOC-230 min prior to trauma. Then the rats in group BOC-2 and BML-111 were injected intraperitoneally with 1 mg/kg of BML-111 immediately and 24 hours after trauma. The neurological severity scores (NSS) were evaluated at 3 and 7 days after brain trauma. The protein expression levels of NLRP3, Caspase-1-p20 and active Caspase-3 were determined by Western blot. The content of IL-1β and IL-18 was detected by ELISA assays. The apoptotic cells were analyzed by the TUNEL method. Results: Compared with group Sham, the brain water content and NSS scores in group TBI were increased, and the protein levels of NLRP3, Caspase-1-p20, activated Caspase-3, IL-1β and IL-18 as well as TUNEL-positive cells in the cortex were elevated significantly (P<0.05); compared with group TBI, the brain water content and NSS scores in group BML-111 were reduced, and the protein levels of NLRP3, Caspase-1-p20, activated Caspase-3, IL-1β and IL-18 as well as TUNEL-positive cells in the cortex were decreased (P<0.05); Compared with group BML-111, the brain water content and NSS scores in group BOC-2 were increased, and the protein levels of NLRP3, Caspase-1-p20, activated Caspase-3, IL-1β and IL-18 as well as TUNEL-positive cells in the cortex were up-regulated (P<0.05). Conclusions: The lipoxin receptor agonist BML-111 might attenuate traumatic brain injury in rats by inhibiting NLRP3 inflammasome activation.