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首页> 外文期刊>Molecular medicine reports >Electroacupuncture at the Baihui acupoint alleviates cognitive impairment and exerts neuroprotective effects by modulating the expression and processing of brain-derived neurotrophic factor in APP/PS1 transgenic mice
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Electroacupuncture at the Baihui acupoint alleviates cognitive impairment and exerts neuroprotective effects by modulating the expression and processing of brain-derived neurotrophic factor in APP/PS1 transgenic mice

机译:百会穴电针通过调节APP / PS1转基因小鼠脑源性神经营养因子的表达和加工,减轻认知障碍,发挥神经保护作用。

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摘要

Alzheimer's disease (AD) is a common human neurodegenerative disorder characterized by progressive deterioration of cognition and memory. Acupuncture at the Baihui (DU20) acupoint has long been used in China to clinically treat cognitive impairment. However, the precise mechanism underlying its neuroprotective effects remains to be elucidated. In the present study, electroacupuncture (EA) at the Baihui (DU20) acupoint was observed to markedly ameliorate cognitive impairments, reduce the aberrant overexpression of beta-amyloid(1-42), and inhibit neuronal apoptosis in APP/PS1 mice. As brain-derived neurotrophic factor (BDNF) has been implicated in the pathogenesis of AD, the expression and processing of BDNF in APP/PS1 mice was investigated. EA at the Baihui (DU20) acupoint was indicated to significantly enhance the expression levels of mature BDNF and proBDNF in APP/PS1 mice. Furthermore, an increase in the BDNF/proBDNF ratio, upregulation of the expression levels of phosphorylated tropomyosin receptor kinase B and a decrease in the expression level of p75 neurotrophin receptor were also observed in the APP/PS1 mice. The present study demonstrates the efficacy of EA at the Baihui (DU20) acupoint in the treatment of cognitive impairments in APP/PS1 transgenic mice. The present study hypothesized that modulation of BDNF expression and processing may be the underlying mechanism by which stimulation of the Baihui (DU20) acupoint exerts its neuroprotective effect.
机译:阿尔茨海默氏病(AD)是一种常见的人类神经退行性疾病,其特征是认知和记忆力逐渐下降。在中国,百会穴(DU20)穴位针灸一直被用于临床治疗认知障碍。但是,其神经保护作用的确切机制尚待阐明。在本研究中,观察到百会穴(DU20)的电针(EA)可以显着改善认知障碍,减少β-淀粉样蛋白(1-42)的异常过表达,并抑制APP / PS1小鼠的神经元凋亡。由于脑源性神经营养因子(BDNF)参与了AD的发病机制,因此研究了BDNF在APP / PS1小鼠中的表达和加工。指示百会穴(DU20)上的EA可以显着增强APP / PS1小鼠中成熟BDNF和proBDNF的表达水平。此外,在APP / PS1小鼠中还观察到BDNF / proBDNF比的增加,磷酸化的原肌球蛋白受体激酶B的表达水平的上调和p75神经营养蛋白受体的表达水平的降低。本研究证明了百会穴(DU20)上的EA在APP / PS1转基因小鼠认知障碍的治疗中的功效。本研究假设BDNF表达和加工的调节可能是刺激百会穴(DU20)发挥神经保护作用的潜在机制。

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