Parkinson's disease is a
neurodegenerative disorder of uncertain pathogenesis characterized by a loss of dopaminergic neurons in substantia nigra pars compacta, and can be modeled by the
neurotoxin 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (
MPTP). Oxidative stress may contribute to
MPTP- and
Parkinson's disease-related neurodegeneration.
Fucoidan is a sulfated
polysaccharide extracted from brown seaweeds which possesses a wide variety of biological activities including potent antioxidative effects. Here we investigated the effect of
fucoidan treatment on locomoter activities of animals, striatal
dopamine and its metabolites and survival of nigral dopaminergic neurons in
MPTP-induced animal model of
Parkinsonism in C57/BL mice in vivo and on the neuronal damage induced by
1-methyl-4-phenylpyridinium (MPP(+)) in vitro, and to study the possible mechanisms. When administered prior to
MPTP,
fucoidan reduced behavioral deficits, increased striatal
dopamine and its metabolites levels, reduced cell death, and led to a marked increase in
tyrosine hydroxylase expression relative to mice treated with
MPTP alone. Furthermore, we found that
fucoidan inhibited
MPTP-induced lipid peroxidation and reduction of
antioxidant enzyme activity. In addition, pre-treatment with
fucoidan significantly protected against MPP(+)-induced damage in MN9D cells. Taken together, these findings suggest that
fucoidan has protective effect in
MPTP-induced neurotoxicity in this model of
Parkinson's disease via its antioxidative activity.