Neural Regeneration Research ›› 2012, Vol. 7 ›› Issue (14): 1080-1087.

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Anti-parkinsonian effects of octacosanol in 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine-treated mice

Tao Wang1, Yanyong Liu2, Nan Yang2, Chao Ji2, Piu Chan1, Pingping Zuo2   

  1. 1  Department of Neurobiology, Beijing Institute of Geriatrics, Xuanwu Hospital of Capital Medical University, Beijing 100053, China
    2  Department of Pharmacology, Institute of Basic Medical Sciences, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing 100005, China
  • Received:2011-11-01 Revised:2012-02-24 Online:2012-05-15 Published:2012-05-15
  • Contact: Pingping Zuo, Ph.D., Professor, Department of Pharmacology, Institute of Basic Medical Sciences, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing 100005, China; Piu Chan, Department of Neurobiology, Beijing Institute of Geriatrics, Xuanwu Hospital of Capital Medical University, Beijing 100053, China pingping_zuo@126.com;pbchan90@gmail.com
  • About author:Tao Wang☆, M.D., Assistant professor, Department of Neurobiology, Beijing Institute of Geriatrics, Xuanwu Hospital of Capital Medical University, Beijing 100053, China. Tao Wang and Yanyong Liu contributed equally to this study.

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Abstract:

Our previous research showed that octacosanol exerted its protective effects in 6-hydroxydopamine-induced Parkinsonian rats. The goal of this study was to investigate whether octacosanol would attenuate neurotoxicity in 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP)-treated C57BL/6N mice and its potential mechanism. Behavioral tests, tyrosine hydroxylase immunohistochemistry and western blot were used to investigate the effects of octacosanol in a mouse model of Parkinson’s disease. Oral administration of octacosanol
(100 mg/kg) significantly improved behavioral impairments in mice treated by MPTP and markedly ameliorated morphological appearances of tyrosine hydroxylase-positive neuronal cells in the substantia nigra. Furthermore, octacosanol blocked MPTP-induced phosphorylation of p38MAPK and JNK, but not ERK1/2. These findings implicated that the protective effects afforded by octacosanol might be mediated by blocking the phosphorylation of p38MAPK and JNK on the signal transduction in vivo. Considering its excellent tolerability, octacosanol might be considered as a candidate agent for clinical application in treating Parkinson’s disease.

Key words: Parkinson’s disease, neuroprotecion, mitogen-activated protein kinase, c-Jun N-terminal kinase, p38MAPK, substantia nigra, neural regeneration