The Effect of Fucoidan on Cellular Oxidative Stress and the CatD-Bax Signaling Axis in MN9D Cells Damaged by 1-Methyl-4-Phenypyridinium.

The purpose of this study was to investigate the impact of fucoidan (FUC) on the oxidative stress response and lysosomal apoptotic pathways in the Parkinson disease (PD) cell model. The Dopaminergic nerve precursor cell line(MN9D) cells that served as a PD model in this study underwent damage induced by 100 μM 1-methyl-4-phenyl pyridine (MPP). Cell viability was assessed after FUC treatment and intracellular SOD GSH was measured via immunofluorescence assay. Cellular changes in cathepsin D, Autophagy marker Light Chain 3-II (LC3-II), and apoptotic protein Bax were assessed by Western blot. The expression of Cat D, LC3-II, and B cell lymphoma-2-associated x protein (Bax) was also measured after addition of the cathepsin inhibitor, pepstatin A. The results indicated that MN9D cell viability decreased by 50% within 24 h after 100 μM MPP induced toxicity. Pretreatment with 100 μM Fucoidan reduced cellular expression of LC3-II and CatD in 3 h and suppressed the induction of Bax protein. After pepstatin A treatment, Bax expression was significantly downregulated.FUC reversed the reduction of superoxide dismutase (SOD) L-Glutathione(GSH), decreased cell viability, and apoptosis induced by MPP in 6 h, suggesting that Fucoidan can attenuate damage to MN9D cells induced by MPP. Fucoidan protected lysosomes, reduced the expression of LC3-II, inhibited the expression of CatD-Bax and the oxidative stress response, suppressed apoptosis, and thus conferred protective effects for dopaminergic neural cells. FUC may have neuroprotective effects on PD and further research is needed.