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Electroacupuncture improves cognitive deficits and activates PPAR-γ in a rat model of Alzheimer's disease
  1. Min Zhang1,2,
  2. Gui-Hua Xv1,
  3. Wei-Xin Wang3,
  4. Di-Juan Meng1,
  5. Yan Ji4
  1. 1Nursing College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China
  2. 2Medical College of Jiangsu University, Zhenjiang, Jiangsu Province, China
  3. 3Department of General Surgery, the Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu Province, China
  4. 4Nursing College, Nanjing Medical University, Nanjing, Jiangsu Province, China
  1. Correspondence to Professor Gui-Hua Xv, Nursing College, Nanjing University of Chinese Medicine, No. 138 Xianlin Road, Xianlin University City, Nanjing, Jiangsu Province 210023, China; xgh_88{at}; zhangmin0922234{at}


Background Alzheimer's disease (AD) is an age-associated neurodegenerative disorder that is associated with a progressive impairment of cognition. Acupuncture has protective effects, although the molecular mechanisms are largely unknown. The activation of peroxisome proliferator activated receptor γ (PPAR-γ) has an impact on the pathogenesis of AD.

Objective To test the hypothesis that electroacupuncture (EA) confers therapeutic benefits through activation of PPAR-γ in a rat model of AD.

Methods 80 male Sprague-Dawley rats were randomly divided into four groups (n=20 each): Control (healthy control group), Sham (sham-operated group), AD (untreated AD model group), and AD+EA (AD model group treated with EA). The AD model was induced in the latter two groups by injection of amyloid-β (Aβ)1-40 into the hippocampal CA1 area bilaterally. EA was administered at GV20 and BL23 six times per week for 4 weeks. The rats’ behaviour was examined using the Morris water maze test, and protein expression of Aβ, hyperphosphorylated tau protein (p-Tau), PPAR-γ, and hyperphosphorylated p38 mitogen activated protein kinase (p38MAPK) in the hippocampal CA1 region was examined by immunohistochemistry and Western blotting.

Results EA significantly improved cognitive deficits and reduced Aβ and p-Tau Ser404 protein concentrations in the hippocampal CA1 region. AD decreased PPAR-γ and increased p-p38MAPK, while EA significantly upregulated PPAR-γ expression and significantly downregulated p-p38MAPK expression.

Conclusions Acupuncture at GV20 and BL23 might have a beneficial effect on rats with AD via activation of PPAR-γ and inhibition of p-p38MAPK expression.


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