Tic disorder is a class of nervous system diseases characterized by involuntary muscle contraction, and its pathogenesis is complex. This study aimed to investigate the mechanism of action of GFAP in tic disorder and its potential influence on neuroprotection and behavior improvement. The expression level of GFAP in brain tissues of each group was detected by immunohistochemistry, and the changes of tic behavior were evaluated by behavioral tests. Western blot and RT-PCR were used to detect the expression of GFAP and related signaling pathway proteins and mRNA, in order to reveal the molecular mechanism of GFAP. Behavioral tests showed that the frequency and intensity of convulsions in the GFAP intervention group were lower than those in the non-intervention group, indicating that GFAP had a certain neuroprotective effect. Through molecular biological analysis, we found that GFAP may exert its neuroprotective effects by modulating signaling pathways related to inflammatory responses, for example, the NF- κ B signaling pathway. The GFAP intervention group was also significantly lower in the level of neuronal damage markers than in the no-intervention group, which further confirmed the neuroprotective effect of GFAP.