Neural Regeneration Research ›› 2012, Vol. 7 ›› Issue (3): 165-170.

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Anchanling reduces pathology in a lactacystin- induced Parkinson's disease model

Yinghong Li1, Zhengzhi Wu1, 2, Xiaowei Gao1, Qingwei Zhu1, Yu Jin1, Anmin Wu1, Andrew C. J. Huang3   

  1. 1 Shenzhen Second People’s Hospital, First Affiliated Hospital of Shenzhen University, Shenzhen 518035, Guangdong Province, China
    2 Shenzhen Institute of Gerontology, Second Clinical Medical College, Jinan University, Shenzhen 518020, Guangdong Province, China
    3 Larry Hillblom Islet Research Center, David Geffen School of Medicine, UCLA, Los Angeles, CA 90024, USA
  • Received:2011-06-02 Revised:2011-12-20 Online:2012-01-25 Published:2012-01-25
  • Contact: Zhengzhi Wu, Professor, Investigator, Doctoral supervisor, Shenzhen Second People’s Hospital, First Affiliated Hospital of Shenzhen University, Shenzhen 518035, Guangdong Province, China; Shenzhen Institute of Gerontology, Second Clinical Medical College, Jinan University, Shenzhen 518020, Guangdong Province, China zhengzhw@yahoo.com.cn
  • About author:Yinghong Li☆, Doctor, Associate professor, Shenzhen Second People’s Hospital, First Affiliated Hospital of Shenzhen University, Shenzhen 518035, Guangdong Province, China

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Abstract:

A rat model of Parkinson's disease was induced by injecting lactacystin stereotaxically into the left mesencephalic ventral tegmental area and substantia nigra pars compacta. After rats were intragastrically perfused with Anchanling, a Chinese medicine, mainly composed of magnolol, for 5 weeks, when compared with Parkinson’s disease model rats, tyrosine hydroxylase expression was increased, α-synuclein and ubiquitin expression was decreased, substantia nigra cell apoptosis was reduced, and apomorphine-induced rotational behavior was improved. Results suggested that Anchanling can ameliorate Parkinson's disease pathology possibly by enhancing degradation activity of the ubiquitin-proteasome system.

Key words: Parkinson's disease, Anchanling, ubiquitin-proteasome system, α-synuclein, tyrosine hydroxylase, cell apoptosis