%0 Journal Article
%T Magnolol Protects against MPTP/MPP+-Induced Toxicity via Inhibition of Oxidative Stress in In Vivo and In Vitro Models of Parkinson¡¯s Disease
%A Akiko Muroyama
%A Aya Fujita
%A Cheng Lv
%A Shota Kobayashi
%A Yoshiyasu Fukuyama
%A Yasuhide Mitsumoto
%J Parkinson's Disease
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/985157
%X The aim of this study is to investigate the role of magnolol in preventing 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP-) induced neurodegeneration in mice and 1-methyl-4-phenylpyridinium ion-(MPP+-) induced cytotoxicity to human neuroblastoma SH-SY5Y cells and to examine the possible mechanisms. Magnolol (30£¿mg/kg) was orally administered to C57BL/6N mice once a day for 4 or 5 days either before or after MPTP treatment. Western blot analysis revealed that MPTP injections substantially decreased protein levels of dopamine transporter (DAT) and tyrosine hydroxylase (TH) and increased glial fibrillary acidic protein (GFAP) levels in the striatum. Both treatments with magnolol significantly attenuated MPTP-induced decrease in DAT and TH protein levels in the striatum. However, these treatments did not affect MPTP-induced increase in GFAP levels. Moreover, oral administration of magnolol almost completely prevented MPTP-induced lipid peroxidation in the striatum. In human neuroblastoma SH-SY5Y cells, magnolol significantly attenuated MPP+-induced cytotoxicity and the production of reactive oxygen species. These results suggest that magnolol has protective effects via an antioxidative mechanism in both in vivo and in vitro models of Parkinson¡¯s disease. 1. Introduction Parkinson¡¯s disease (PD) is a progressive neurodegenerative disorder characterized by the selective loss of nigral dopaminergic neurons resulting in reduced striatal dopamine and the cardinal clinical features such as bradykinesia, resting tremor, rigidity, and postural instability [1]. Currently, pharmacotherapy and surgical approaches for the treatments of PD can only improve the neurological symptoms [2]. Furthermore, long-term treatment with the dopamine precursor levodopa often leads to the development of debilitating dyskinesias [2]. Therefore, to search neuroprotective therapies using pharmacological and nonpharmacological approaches could be important to delay the progression of pathogenesis in PD. The cause of PD remains unknown, but a valuable clue has been suggested by discovery of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; [3]). MPTP selectively damages the dopaminergic pathways in a pattern similar to that seen in PD and induces a parkinsonian syndrome in humans, monkeys, and mice [1, 4, 5]. The discovery that MPTP acts through inhibition of complex I of the electron transport chain stimulated study of mitochondrial function in the brains from patients with PD [6, 7]. Mizuno et al. [8] proposed that energy crisis is the most important mechanism of nigral cell death
%U http://www.hindawi.com/journals/pd/2012/985157/