Abstract: Objective　To investigate the protective effects of MCC950 on traumatic brain injury (TBI) mice by inhibiting pyroptosis via suppressing NLRP3 inflammasome.　Methods　A total of 36 BALB/c mice were randomly divided into the following groups: a sham injury group, a TBI model group, a MCC950 1-day and 7-day treatment group. The TBI model of mice was induced by free fall method, and MCC950 was intraperitoneally injected into the treatment group after modeling. HE staining and nissl staining were used to evaluate the brain tissue injury conditions of each group. The expressions of NLRP3, Caspase1 and GSDMD in each group were detected by the immunofluorescence.　Results　H&E staining showed that compared with the sham injury group, the number of neurons in the injured area in the TBI model group decreased, and the nuclei of neurons were consolidated and hyperchromatic, with a large number of vacuoles around the nuclei. The neuron status of the TBI+MCC950 treatment group (1-day and 7-day treatment group) were significantly better than that of the TBI model group. Nissl staining showed that compared with the TBI model group, the neuron loss and injury in the TBI+MCC950 treatment group (1-day and 7-day treatment group) attenuated. Immunofluorescence showed that compared with the TBI model group, the expression levels of NLRP3, caspase1 and GSDMD in frozen sections of brain tissues of the TBI+MCC950 group (1-day and 7-day treatment group) significantly reduced.　Conclusions　Application of MCC950 in the treatment of TBI mice can effectively inhibit NLRP3-mediated pyroptosis and alleviate the damage of brain tissue and cell structure at the wound site.

Key words: Traumatic brain injury, 　NLRP3 inflammasome, 　Pyroptosis；　MCC950