关键词: 帕金森病, 1-甲基-4-苯基吡啶离子, 褐藻多糖硫酸酯, 神经保护

Abstract: Objective To study the neuroprotective effect and mechanism of fucoidan against MPP⁺-induced MN9D cell damage. Methods The MN9D cell damage model was induced by treating MN9D cells with different concentrations (25, 50, 100, 200 μmol/L) of MPP⁺ for 36 h and with 50 μmol/L MPP⁺ for different time course(12, 24, 36, 48 h). To explore the neuroprotective effects of fucoidan, the cells were pretreated with 0.01, 0.1, 1.0 g/L fucoidan for 1 h, followed by co-treatment with 50 μmol/L MPP⁺ for 36 h. The viability of MN9D cells was detected by MTT conversion and LDH leakage. Furthermore, we detected the generation of reactive oxygen species in MN9D cells to understand the underlying mechanism of the neuroprotective effects of fucoidan. Results After being treated with different concentrations of MPP⁺ for 36 h or with 50 μmol/L MPP⁺ for different time course, the cell viability of MN9D cells decreased significantly; 50 μmol/L MPP⁺ treatment for 36 h induced a significant decrease in MTT metabolic rate and an increase in LDH leakage rate in the MN9D cells. 0.1, 1.0 g/L fucoidan pretreatment inhibited MPP⁺-induced cell death and significantly inhibited the generation of reactive oxygen species induced by MPP⁺. Conclusion Fucoidan can protect MN9D cell from the death induced by MPP⁺, and the underlying mechanism may involve the antioxidant capacity of fucoidan.

Key words: Pakinson’s disease, 1-methyl-4-phenylpyridinium, fucoidan, neuroprotective effect