Abstract
Background: The most important therapeutic goals for improving the condition of patients with neurodegenerative diseases are to prevent neuronal cell death and replace damaged cells with cell transplantation. Recently, the use of flavonoids has attracted the attention of researchers due to their anti-inflammatory and neuroprotective effects and with the aim of preventing cell death and promoting cell differentiation. In the present study, the effects of fisetin as a flavonoid were investigated on the prevention of oligodendrocyte death and serum levels of TGF-β in a toxic model of brain myelin destruction.
Methods: C57BL/6 mice were divided into control, sham, cuprizone, fisetin, and cuprizone-fisetin groups. Oligodendrocyte death was induced using cuprizone. Additionally, fisetin was used at a dose of 20 mg/kg in the treated groups. Finally, immunohistochemical staining was used to examine oligodendrocyte markers and ELISA was used to assess serum levels of TGF-β. The results were evaluated and compared using One Way ANOVA.
Findings: The mean serum levels of TGF-β and the mean percentage of MOG and Olig2 positive cells in the fisetin-treated groups were significantly increased compared to the cuprizone group (P ≤0.05, P ≤0.05 and P ≤0.01, respectively).
Conclusion: Oligodendrocyte cell death caused by exposure to toxic agents such as cuprizone can be suppressed by flavonoids such as fisetin. Fisetin can maintain the oligodendrocyte population and prevent the development of neurodegenerative diseases by exerting anti-inflammatory and neuroprotective effects.