Zhang Min, Xv Gui-Hua, Wang Wei-Xin, Meng Di-Juan, Ji Yan
Nursing College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China.
Medical College of Jiangsu University, Zhenjiang, Jiangsu Province, China.
Acupunct Med. 2017 Mar;35(1):44-51. doi: 10.1136/acupmed-2015-010972. Epub 2016 Jul 11.
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.
To test the hypothesis that electroacupuncture (EA) confers therapeutic benefits through activation of PPAR-γ in a rat model of AD.
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.
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.
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.
阿尔茨海默病(AD)是一种与年龄相关的神经退行性疾病,与认知功能的进行性损害有关。针刺具有保护作用,但其分子机制大多未知。过氧化物酶体增殖物激活受体γ(PPAR-γ)的激活对AD的发病机制有影响。
验证电针(EA)通过激活AD大鼠模型中的PPAR-γ发挥治疗作用的假说。
将80只雄性Sprague-Dawley大鼠随机分为四组(每组n = 20):对照组(健康对照组)、假手术组(假手术操作组)、AD组(未治疗的AD模型组)和AD+EA组(接受EA治疗的AD模型组)。后两组通过双侧海马CA1区注射淀粉样β蛋白(Aβ)1-40诱导建立AD模型。每周在GV20和BL23穴位进行6次EA治疗,共4周。采用Morris水迷宫试验检测大鼠行为,并通过免疫组织化学和蛋白质印迹法检测海马CA1区Aβ、磷酸化tau蛋白(p-Tau)、PPAR-γ和磷酸化p38丝裂原活化蛋白激酶(p38MAPK)的蛋白表达。
EA显著改善了认知缺陷,并降低了海马CA1区Aβ和p-Tau Ser404蛋白浓度。AD导致PPAR-γ降低和p-p38MAPK升高,而EA显著上调PPAR-γ表达并显著下调p-p38MAPK表达。
针刺GV20和BL23穴位可能通过激活PPAR-γ和抑制p-p38MAPK表达对AD大鼠产生有益作用。