Promotes Anti-Inflammatory Effects and Regulation of Metabolites in an Animal Model of Cerebellar Ataxia.

Cerebellar ataxia is a neurodegenerative disorder with no definitive treatment. Although previous study demonstrated the neuroprotective effects of (), the mechanisms of . treatment on the neuroinflammatory response, neurotransmission, and related metabolites remain largely unknown. We demonstrated that 3-AP rats treated with 25 mg/kg extracts had improved motor coordination and balance in the accelerated rotarod and rod tests. We showed that the . treatment upregulated the expression of and genes to levels comparable to those in the non-3-AP control group. Interestingly, we also observed a significant correlation between gene expression and rod test performance in the 3-AP saline group, but not in the non-3-AP control or .+3-AP groups, indicating a relationship between gene expression and motor balance in the 3-AP rat model. Additionally, we also found that the . treatment increased mitochondrial COX-IV protein expression and normalized dopamine-serotonin neurotransmission and metabolite levels in the cerebellum of the .+3-AP group compared to the 3-AP saline group. In conclusion, our findings suggest that the . treatment improved motor function in the 3-AP rat model, which was potentially mediated through neuroprotective mechanisms involving TGFB2-Smad3 signaling via normalization of neurotransmission and metabolic pathways.