自身免疫性脑脊髓炎 z-bo 2020-12-18 329

　　Objective To investigate the preventive and therapeutic effects of compound glycyrrhizin (CG) on experimental autoimmune encephalomyelitis (EAE) mice and its effect on JAK2/STAT3/SOCS3 signaling pathway.

　　 Method 50 female C57BL/6 mice were randomly divided into 5 groups: blank group, model group and CG low, medium, and high dose intervention groups, each with 10 mice. EAE models were established in the model group and each CG intervention group. The intervention group was injected intraperitoneally with low, medium, and high doses of CG (15, 30, 60 mg/(kg·d)), and the blank group and model group were injected with equal volume of normal saline. ,Continuously for 14 d. Observe the score, pathological changes and degree of neurological deficit in mice. Western blot method was used to detect the expression of brain tissue protein, and real-time fluorescent quantitative RT-PCR method was used to detect the content of brain tissue mRNA. Compared with the model group, the highest neurological deficit score (P<0.05) and cumulative neurological deficit score (P<0.05) of each CG intervention group were reduced, and the degree of inflammatory cell infiltration and demyelination of spinal cord tissue was reduced, JAK2, STAT3 protein and its mRNA expression decreased (P<0.05), SOCS3 protein and its mRNA expression increased (P<0.05), RORγt mRNA expression decreased (P<0.05), Foxp3 mRNA increased (P<0.05) P<0. 05).

　　 Conclusion CG exerts a preventive effect on EAE mice. The mechanism may be related to the up-regulation of the negative regulatory factor SOCS3, the inhibition of JAK/STAT signal pathway and the influence of Th17/Treg cell balance.