Abstract:

Objective To study mechanism of Fucoidan in neurodegenerative disease by observing its effect on cathepsin B activities and oxidative stress.
Methods After 7 days’ differentiation by 50 μg·L-¹ nerve growth factor(NGF), PC12 cells were exposed to 0.5 mmol/L H₂O₂ for 30 min, and then treated with Fucoidan(10 mg·L^-1). The activities of superoxide dismutase(SOD) and reactive oxygen species(ROS) inside cells of each group were assayed. Cathepsin B activities inside cells were determined after being extracted from dPC12. Human liver cathepsin B activities were tested after being exposed to different concentrations of Fucoidan(0.1, 1, 10, 50, 100 mg·L^-1).
Results After oxidative stress, the activities of ROS inside cells increased to 185.2% of normal control, accompanied by lower SOD activities and higher activities of cathepsin B(236.7%) in cytoplasm. Fucoidan treatment decreased ROS levels without any effect on SOD; furthermore, Fucoidan could inhibit both dPC12 cytoplasm cathepsin B activities and human liver cathepsin B activities.
Conclusion Fucoidan’s suppression on cathepsin B activities contributes to its protective effect against oxidative stress which leads to cell apoptosis.

Key words: Fucoidan, cathepsin B, Alzheimer&rsquo, s disease, oxidative stress