文章摘要
张政超.高良姜素神经保护作用及其机制研究进展[J].安徽医药,待发表.
高良姜素神经保护作用及其机制研究进展
投稿时间:2026-08-27  录用日期:2026-10-15
DOI:
中文关键词: 高良姜素  神经保护  神经退行性疾病  信号通路  分子机制
英文关键词: 
基金项目:广东省自然科学(2022A1515012220);广东省中医药局科研项目(202604301643125100)
作者单位地址
张政超* 广东药科大学 广东省广州市番禺区小谷围街道广东药科大学
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中文摘要:
      神经系统疾病如神经退行性疾病等均为多因素、多环节介导的复杂病理过程,现有治疗手段尚难以有效延缓疾病进展。高良姜素(Galangin)是源自高良姜的天然黄酮类化合物,具有抗氧化、抗炎、抗凋亡及调控自噬等神经保护活性,可通过多条信号通路发挥作用:激活 Nrf2/Keap1 通路以缓解氧化应激,抑制 TLR4/NF-κB、MAPK 通路减轻神经炎症,调控 Bcl-2 家族与 Caspase 级联反应减少神经元凋亡,并经由 PI3K/AKT 通路维持自噬稳态。新近研究表明,miRNA-134/NF-κB 轴与 Shh/Ptch1/Gli1 通路同样参与高良姜素介导的神经修复。本文系统综述高良姜素多靶点神经保护机制的研究进展,探讨其成药性与临床转化面临的挑战,以期为基于高良姜素的神经保护药物研发提供参考。
英文摘要:
      Neurological disorders, such as neurodegenerative diseases, represent complex pathological processes driven by multiple factors and interconnected events, and current therapeutic modalities remain inadequate to effectively retard disease progression. Galangin, a natural flavonoid derived from Alpinia galanga, exerts multifaceted neuroprotective activities—including antioxidant, anti-inflammatory, anti-apoptotic, and autophagy-regulating effects—through diverse signaling pathways: it alleviates oxidative stress by activating the Nrf2/Keap1 pathway, attenuates neuroinflammation by inhibiting the TLR4/NF-κB and MAPK pathways, reduces neuronal apoptosis by modulating the Bcl-2 family and the caspase cascade, and sustains autophagic homeostasis via the PI3K/AKT pathway. Recent studies have demonstrated that the miRNA-134/NF-κB axis and the Shh/Ptch1/Gli1 pathway also participate in galangin-mediated neural repair. This review systematically summarizes the research progress on the multi-target neuroprotective mechanisms of galangin, discusses the challenges concerning its druggability and clinical translation, and aims to provide a reference for the development of galangin-based neuroprotective agents.
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