Effect of pharmacological intervention and pathogenesis discussion about rats with tic disorders

Le résumé fourni par la source

To investigate the pathogenesis of Tic disorders (TD), particularly their relationship with central nervous system inflammation, we conducted an animal experiment. A TD model was established for rats, and their behavior and immune cytokines and receptor in the striatum were compared between a diseased group and healthy control group of rats. After receiving effective drug interventions (the traditional Chinese medicine Jian-Pi-Zhi-Dong decoction (JPZDD) and the Western medicine Tiapride), we observed changes in behavior and immune cytokine and receptor expression in the striatum and analyzed the association between central nervous system inflammation and TD. The results are as follows: (1) Successful modeling: Compared to normal rats, TD diseased rats exhibited increased spontaneous activity, stereotypical exercise, and elevated expression of inflammatory cytokines and receptor in the striatum. (2) Effective pharmacological intervention: Tiapride and JPZDD reduced spontaneous activity, stereotypical exercise, and the expression of inflammatory cytokines and receptor in rats with TD. (3) The number of spontaneous activities and stereotypical exercise scores was positively correlated with central nervous system inflammation. The expression of Toll-like receptor 4 (TLR4), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α) in the striatum of the diseased group rats were significantly greater than those in the striatum of the normal group rats. Effective pharmacological intervention reduced the expression of inflammatory cytokine and receptor in the striatum, bringing them to expression similar to those in normal rats. Based on these results, we conclude that TD is associated with central nervous system inflammation and that the severity of TD is positively correlated with the severity of central nervous system inflammation. We hypothesize that the pathogenesis of TD may involve elevated TLR4, which triggers overactivation of microglia in the brain resulting in the release of excessive IL-6, IL-8, and TNF-α. This process damages neurons and leads to tic symptoms in patients. • Question: Is the onset of Tic disorders related to central nervous system inflammation? • Findings: Excess inflammatory cytokine and microglia damage the central nervous system and lead to the onset of Tic disorders. Drugs with different types of mechanisms of action may exert similar therapeutic effects by inhibiting this pathway. • Meaning: The findings provides the possibility of clarifying the pathogenesis of Tic disorders.

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