Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2011;6(5):e19790.
doi: 10.1371/journal.pone.0019790. Epub 2011 May 23.

The antioxidative effect of electro-acupuncture in a mouse model of Parkinson's disease

Haomin Wang  1 , Yanli Pan, Bing Xue, Xinhong Wang, Feng Zhao, Jun Jia, Xibin Liang, Xiaomin Wang
Affiliations

The antioxidative effect of electro-acupuncture in a mouse model of Parkinson's disease

Haomin Wang et al. PLoS One. 2011.

Abstract

Accumulating evidence indicates that oxidative stress plays a critical role in Parkinson's disease (PD). Our previous work has shown that 100 Hz electro-acupuncture (EA) stimulation at ZUSANLI (ST36) and SANYINJIAO (SP6) protects neurons in the substantia nigra pars compacta from 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity in male C57BL/6 mice, a model of PD. In the present study we administered 100 Hz EA stimulation at the two acupoints to MPTP-lesioned mice for 12 sessions starting from the day prior to the first MPTP injection. We found that in the striatum of MPTP treated mice 100 Hz EA stimulation effectively inhibited the production of hydrogen peroxide and malonaldehyde, and increased glutathione concentration and total superoxide dismutase activity through biochemical methods. However, it decreased glutathione peroxidase activity via biochemical analysis and did not affect the level of 1-methyl-4-phenylpyridinium in the striatum revealed by high performance liquid chromatography with ultraviolet detection. These data suggest that 100 Hz EA stimulation at ST36 and SP6 has antioxidative effects in the MPTP model of PD. This data, along with our previous work, indicates that 100 Hz EA stimulation at ST36 and SP6 protects the nigrostriatal system by multiple mechanisms including antioxidation and antiapoptosis, and suggests that EA stimulation is a promising therapy for treating PD.

PubMed Disclaimer

Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Experimental design of the study.
Numbers represent days.
Figure 2
Figure 2. 100 Hz EA stimulation protects dopaminergic neurons from MPTP toxicity.
(A and B) NS. (C and D) 100 Hz + NS. (E and F) MPTP. (G and H) 0 Hz + MPTP. (I and J) 100 Hz + MPTP. (K) Quantification of TH positive neuronal profiles in the SNpc. *p<0.05, compared with NS group. n = 3. Scale bar, 200 µm (A, C, E, G and I) and 50 µm (B, D, F, H and J).
Figure 3
Figure 3. 100 Hz EA stimulation increases the contents of striatal DA and its metabolites in MPTP-treated mice.
(A) DA. (B) DOPAC. (C) HVA. ***p<0.001, compared with NS group; #p<0.05, compared with MPTP group. n = 6∼9.
Figure 4
Figure 4. 100 Hz EA stimulation inhibits the elevation of striatal H2O2 level in MPTP-treated mice.
*p<0.05, compared with NS group; #p<0.05, compared with MPTP group. n = 5∼8.
Figure 5
Figure 5. 100 Hz EA stimulation effects on the content/activity of GSH, GSH-PX, SOD and MDA in the striatum.
Saline group (gray bar), MPTP group (white bar) and 100 Hz + MPTP group (black bar). (A) GSH content. (B) GSH-PX activity. (C) SOD activity. (D) MDA content. **p<0.01, ***p<0.001, compared with NS group; ##p<0.01, ###p<0.001, compared with MPTP group on the same day. n = 6∼7 (A and B) or n = 5∼7 (C and D).
Figure 6
Figure 6. 100 Hz EA stimulation does not affect MPP+ formation.
MPTP group (white bar) and 100 Hz + MPTP group (black bar). n = 6∼8.
See this image and copyright information in PMC

Comment in

References

    1. Dexter DT, Carter CJ, Wells FR, Javoy-Agid F, Agid Y, et al. Basal lipid peroxidation in substantia nigra is increased in Parkinson's disease. J Neurochem. 1989;52:381–389. - PubMed
    1. Floor E, Wetzel MG. Increased protein oxidation in human substantia nigra pars compacta in comparison with basal ganglia and prefrontal cortex measured with an improved dinitrophenylhydrazine assay. J Neurochem. 1998;70:268–275. - PubMed
    1. Alam ZI, Daniel SE, Lees AJ, Marsden DC, Jenner P, et al. A generalised increase in protein carbonyls in the brain in Parkinson's but not incidental Lewy body disease. J Neurochem. 1997;69:1326–1329. - PubMed
    1. Yoritaka A, Hattori N, Uchida K, Tanaka M, Stadtman ER, et al. Immunohistochemical detection of 4-hydroxynonenal protein adducts in Parkinson disease. Proc Natl Acad Sci U S A. 1996;93:2696–2701. - PMC - PubMed
    1. Shigenaga MK, Ames BN. Assays for 8-hydroxy-2′-deoxyguanosine: a biomarker of in vivo oxidative DNA damage. Free Radic Biol Med. 1991;10:211–216. - PubMed

Publication types

MeSH terms