〔Abstract〕 Objective To construct a rat model of trigeminal neuralgia(TN) to explore the expression of high-mobility group box-1(HMGB1) in the trigeminal ganglion(TG) and the possible mechanism of HMGB1's effect on pain. Methods TN model was constructed by infraorbital nerve constriction and divided into operation group(CCI group) and Sham group, and the success of the model construction was determined through mechanical pain threshold assessment. Real time fluorescence quantitative PCR(RT-qPCR) and Western blot were used to detect high mobility group protein B1(HMGB1), Toll receptor 4(TLR4), and Nuclear Factor Kappa B(NF-κB) mRNA and protein expression in the ipsilateral trigeminal ganglion(TG) of the Sham and CCI rats. 50 mg/kg HMGB1 inhibitor glycyrrhizin(GL) was injected intraperitoneally every day for two weeks, and normal saline(NS) was used as control. The patients were divided into CCI group, CCI+NS group and CCI+GL group. HMGB1, TLR4, and NF-κB mRNA and protein expression in the ipsilateral trigeminal ganglion(TG) were detected by RT-qPCR and Western blot in CCI group, CCI+NS group, and CCI+GL group. Results The mechanical threshold on the operated side of the rat continued to decrease(P<0.05), and mechanical pain threshold identification model was successfully constructed. After chronic compressive injury to the infraorbital nerve in rats, HMGB1, TLR4, and NF-κB mRNA and protein expression in TG on the operated side increased(P<0.05); After administration of HMGB1 inhibitor Glcyrrhizin, HMGB1, TLR4, NF-κB showed a decrease(P<0.05). Conclusion HMGB1 is associated with TN, and HMGB1 may be involved in the pathogenesis of TN through TLR4/NF-κB signaling pathway.