Electroacupuncture remediates glial dysfunction and ameliorates neurodegeneration in the astrocytic α-synuclein mutant mouse model

Journal of Neuroinflammation

Xiaomin Wang²  Jun Jia²  Jiazeng Wang²  Xibin Liang¹  Wenzhong Zhang²  Xiaoli Gong²  Jian Yang²  E Lv²  Jiahui Deng² 

[1] Department of Neurology and Neurological Sciences, Stanford University, Stanford 94305, CA, USA;Departments of Neurobiology and Physiology, Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Beijing Key Laboratory for Parkinson’s Disease, Capital Medical University; Beijing Institute for Brain Disorders, Beijing 100069, China

关键词: Nrf2;    Glial dysfunction;    Electroacupuncture;    α-synuclein;    Astrogliosis;   

Others  :  1221983
DOI  :  10.1186/s12974-015-0302-z

 received in 2015-01-08, accepted in 2015-04-16,  发布年份 2015

【 摘 要 】

Background

The acupuncture or electroacupuncture (EA) shows the therapeutic effect on various neurodegenerative diseases. This effect was thought to be partially achieved by its ability to alleviate existing neuroinflammation and glial dysfunction. In this study, we systematically investigated the effect of EA on abnormal neurochemical changes and motor symptoms in a mouse neurodegenerative disease model.

Methods

The transgenic mouse which expresses a mutant α-synuclein (α-syn) protein, A53T α-syn, in brain astrocytic cells was used. These mice exhibit extensive neuroinflammatory and motor phenotypes of neurodegenerative disorders. In this study, the effects of EA on these phenotypic changes were examined in these mice.

Results

EA improved the movement detected in multiple motor tests in A53T mutant mice. At the cellular level, EA significantly reduced the activation of microglia and prevented the loss of dopaminergic neurons in the midbrain and motor neurons in the spinal cord. At the molecular level, EA suppressed the abnormal elevation of proinflammatory factors (tumor necrosis factor-α and interleukin-1β) in the striatum and midbrain of A53T mice. In contrast, EA increased striatal and midbrain expression of a transcription factor, nuclear factor E2-related factor 2, and its downstream antioxidants (heme oxygenase-1 and glutamate-cysteine ligase modifier subunits).

Conclusions

These results suggest that EA possesses the ability to ameliorate mutant α-syn-induced motor abnormalities. This ability may be due to that EA enhances both anti-inflammatory and antioxidant activities and suppresses aberrant glial activation in the diseased sites of brains.

【 授权许可】

   
2015 Deng et al.; licensee BioMed Central.

【 图 表 】

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