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

Abstract

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/kgextracts had improved motor coordination and balance in the accelerated rotarod and rod tests. We showed that the. treatment upregulated the expression ofandgenes to levels comparable to those in the non-3-AP control group. Interestingly, we also observed a significant correlation betweengene 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 betweengene 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.