中医药调控PI3K/AKT信号通路治疗阿尔茨海默症的研究进展
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1.江西中医药大学药学院;2.江中药业股份有限公司

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江西省自然科学基金资助项目(20244BAB28017)


Research Progress on the Modulation of the PI3K/AKT Signaling Pathway in the Treatment of Alzheimer's Disease with Traditional Chinese Medicine
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1.School of Pharmacy,Jiangxi University of Chinese Medicinel;2.Jiangzhong Pharmaceutical Co.,Ltd;3.School of Pharmacy,Jiangxi University of Chinese Medicine

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    摘要:

    阿尔茨海默症(Alzheimer’s disease,AD)是全球最常见的神经退行性疾病,主要特征包括认知障碍和记忆功能紊乱,其病理机制涉及β-淀粉样蛋白(amyloid β-protein,Aβ)毒性沉积、Tau蛋白过度磷酸化导致的神经原纤维缠结(neurofibrillary tangles,NFTs)、线粒体功能障碍、突触功能障碍、胆碱能系统功能障碍、神经炎症以及氧化应激等。目前,临床用于治疗AD的药物有乙酰胆碱酯酶抑制剂、NMDA拮抗剂,虽然对认知功能有一定的改善,但不能延缓病情,且有副作用。研究表明,中医药可以调控磷脂酰肌醇3-激酶/蛋白激酶B(phosphatidylinositol 3-kinase/protein kinase B,PI3K/AKT)信号通路对AD产生治疗作用。通过对近年来国内外文献进行整理,将中药单体成分、提取物以及中药复方调控PI3K/AKT信号通路治疗AD的机制进行总结,以期为中医药治疗AD提供一定的理论基础。

    Abstract:

    Alzheimer’s disease (AD) is the most common neurodegenerative disorder worldwide, primarily characterized by cognitive impairment and memory dysfunction. Its pathological mechanisms include the toxic deposition of amyloid β-protein (Aβ), neurofibrillary tangles (NFTs) caused by excessive phosphorylation of Tau protein, mitochondrial dysfunction, synaptic impairment, cholinergic system dysfunction, neuroinflammation, and oxidative stress. Current clinical treatments for AD, such as acetylcholinesterase inhibitors and NMDA receptor antagonists, can provide some cognitive benefits but fail to slow disease progression and often cause side effects. Recent studies have shown that traditional Chinese medicine (TCM) can exert therapeutic effects on AD by regulating the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. This review systematically summarizes research on how TCM, including active compounds, herbal extracts, and formulae, modulates the PI3K/AKT pathway in AD treatment. By integrating recent findings from both domestic and international studies, this paper aims to provide a theoretical foundation for the application of TCM in AD therapy.

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  • 收稿日期:2025-04-01
  • 最后修改日期:2025-04-14
  • 录用日期:2025-05-26
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