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Evidence-Based Complementary and Alternative Medicine
Volume 2014, Article ID 729195, 11 pages
http://dx.doi.org/10.1155/2014/729195
Research Article

Da-Bu-Yin-Wan and Qian-Zheng-San to Neuroprotect the Mouse Model of Parkinson’s Disease

1Department of Anatomy, School of Preclinical Medicine, Beijing University of Chinese Medicine, No. 11 N. 3rd Ring Eastern Road, Beijing 100029, China
2Center of Scientific Research, School of Preclinical Medicine, Beijing University of Chinese Medicine, No. 11 N. 3rd Ring Eastern Road, Beijing 100029, China

Received 16 September 2014; Accepted 3 December 2014; Published 24 December 2014

Academic Editor: Kuttulebbai N. S. Sirajudeen

Copyright © 2014 Xiao-Gang Gong et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Da-Bu-Yin-Wan (DBYW) and Qian-Zheng-San (QZS), two classic traditional Chinese medicinal formulas, were clinically employed to treat Parkinson’s disease (PD). Our previous studies demonstrated neuroprotective effects of them on mitochondrial function in PD mice induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The purpose of this research was to investigate their possible mechanisms in the light of mitochondrial ATP-sensitive potassium (mitoK) channels. The neuroprotective effect of DBYW and QZS on dopamine (DA) neurons in substantia nigra (SN) in the MPTP-induced PD mice was investigated by behavioral test (pole test) and immunohistochemistry. Adenosine triphosphate (ATP) level in the midbrain tissue was detected by firefly luciferase method. MitoK channel subunits SUR1 and Kir6.2 mRNA and protein expressions were tested by real-time PCR (RT-PCR) and Western blot. It was observed that DBYW and/or QZS served to ameliorate MPTP-induced behavioral impairment and prevent the loss of substantia nigra dopamine neurons, as well as increase ATP level in the midbrain tissue and downregulate SUR1 expression at mRNA and protein levels with no marked influence on Kir6.2. We concluded that DBYW and QZS exhibit neuroprotective effects probably through the regulation of ATP level and mitoK channel subunit expressions.