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

AbstractBACKGROUND:
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.
AuthorsJiahui Deng, E Lv, Jian Yang, Xiaoli Gong, Wenzhong Zhang, Xibin Liang, Jiazeng Wang, Jun Jia, Xiaomin Wang
JournalJournal of neuroinflammation (J Neuroinflammation) Vol. 12 Pg. 103 (May 28 2015) ISSN: 1742-2094 [Electronic] England
PMID26016857 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Aif1 protein, mouse
  • Calcium-Binding Proteins
  • Glial Fibrillary Acidic Protein
  • Membrane Proteins
  • Microfilament Proteins
  • NF-E2-Related Factor 2
  • Nfe2l2 protein, mouse
  • alpha-Synuclein
  • Heme Oxygenase-1
  • Hmox1 protein, mouse
  • GCLM protein, mouse
  • Glutamate-Cysteine Ligase
Topics
  • Animals
  • Astrocytes (metabolism)
  • Calcium-Binding Proteins (metabolism)
  • Electroacupuncture (methods)
  • Exploratory Behavior (physiology)
  • Gait Disorders, Neurologic (etiology, therapy)
  • Gene Expression Regulation (drug effects, genetics)
  • Glial Fibrillary Acidic Protein (genetics, metabolism)
  • Glutamate-Cysteine Ligase (genetics, metabolism)
  • Heme Oxygenase-1 (genetics, metabolism)
  • Membrane Proteins (genetics, metabolism)
  • Mice
  • Mice, Transgenic
  • Microfilament Proteins (metabolism)
  • Motor Activity (drug effects, genetics)
  • Motor Neurons (drug effects, metabolism, pathology)
  • Muscle Strength (genetics, physiology)
  • Mutation (genetics)
  • NF-E2-Related Factor 2 (genetics, metabolism)
  • Neurodegenerative Diseases (genetics, pathology, therapy)
  • Spinal Cord (pathology)
  • alpha-Synuclein (genetics)

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