Conclusion
The present study provided evidence for the neuroprotective effects of ChA on cuprizone-induced demyelination and behavioral dysfunction in C57BL/6 mice, possibly by modulating TNFα secretion and BDNF expression.
Methods
The mice received normal diets (Control group: CNT), or Cuprizone-supplemented diets either without ChA (Cuprizone group: CPZ) or with low or high (300, 600 mg/kg/day) doses of ChA (ChA-treated groups: CPZ+ChA300/600). Brain-derived neurotrophic factor (BDNF) and tumor necrosis factor alpha (TNFα) levels, demyelination scores in the corpus callosum (CC), and cognitive impairment were evaluated using the enzyme-linked immunosorbent assay, histological, and Y-maze tests, respectively.
Results
The findings showed that ChA Co-treatment significantly reduced the extent of demyelination in the CC and the serum and brain levels of TNFα in the ChA-treated groups compared to the CPZ group. Besides, treatment with a higher dose of ChA significantly improved the behavioral responses and BDNF levels in the serum and brain of the CPZ+ChA600 group when compared with the CPZ group.