Protective Effect of Chinonin in MPTP-Induced C57BL/6 Mouse Model of Parkinson’s Disease

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  • Feng Guoshuai
    College of Pharmacy, Jinan University
  • Zhang Zhijian
    College of Pharmacy, Jinan University
  • Bao Qingqing
    The Children’s Hospital Zhejiang University School of Medicine
  • Zhang Zaijun
    College of Pharmacy, Jinan University
  • Zhou Libing
    The Joint Laboratory for Brain Function and Health (BFAH), Jinan University and The University of Hong Kong, Medical School of Jinan University
  • Jiang Jie
    College of Pharmacy, Jinan University DongGuan Institute of Jinan University
  • Li Sha
    Department of Pharmaceutics, College of Pharmacy, Jinan University

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The aims of this study were to investigate the effect of chinonin in preventing 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurodegeneration in C57BL/6 mice and to examine the possible mechanisms. The neurotoxin MPTP was employed to create a subacute Parkinson’s disease (PD)-like model in C57BL/6 mice. Chinonin (10, 20, 40 mg/kg body weight) was intraperitoneally administered 0.5 h after MPTP (30 mg/kg) injection for 7 d consecutively. Chinonin showed neuroprotective effects in the MPTP-treated mice PD model by ameliorating motor impairment in the catwalk and open-field tests. Consistently, chinonin reduced loss of dopaminergic neurons in the substantia nigra and prevented depletion of dopamine and its metabolites 3-methoxy-4-hydroxy-phenylacetic acid and homovanillic acid in the striatum of mice. Compared with the MPTP group, in the chinonin plus MPTP groups significant increases of superoxide dismutase activity and glutathione levels were observed as well as a distinct reduction of lipid peroxidation product malondialdehyde in the striatum. Taken together, we propose that chinonin exerts neuroprotective effects in C57BL/6 mouse model of PD and these effects may be due to chinonin’s antioxidative property.

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