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The role of HMGB1 in trigeminal neuralgia / 安徽医科大学学报
Article em Zh | WPRIM | ID: wpr-1032226
Biblioteca responsável: WPRO
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 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 thresh old 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 inhibi tor glycyrrhizin (GL) was inj ected intraperitoneally every day for two week s , 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 West ern 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 success fully 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 associat ed with TN , and HMGB1 may be involved in the pathogenesis of TN through TLR4/NF-κB signaling pathway.
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Base de dados: WPRIM Idioma: Zh Ano de publicação: 2024 Tipo de documento: Article
Buscar no Google
Base de dados: WPRIM Idioma: Zh Ano de publicação: 2024 Tipo de documento: Article