Amin Md Al, Zehravi Mehrukh, Sweilam Sherouk Hussein, Shatu Mst Maharunnasa, Durgawale Trupti Pratik, Qureshi Mohammad Shamim, Durgapal Sumit, Haque M Akiful, Vodeti Rajeshwar, Panigrahy Uttam Prasad, Ahmad Irfan, Khan Sharuk L, Emran Talha Bin
Department of Pharmacy, Faculty of Health and Life Sciences, Daffodil International University, Dhaka 1216, Bangladesh.
Department of Clinical Pharmacy, College of Dentistry & Pharmacy, Buraydah Private Colleges, Buraydah 51418, Saudi Arabia.
Brain Res. 2025 Aug 1;1860:149693. doi: 10.1016/j.brainres.2025.149693. Epub 2025 May 9.
Neurodegenerative diseases (NDs) such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis pose significant challenges due to their complex pathophysiology and lack of effective treatments. Green tea, rich in the epigallocatechin gallate (EGCG) polyphenolic component, has demonstrated potential as a neuroprotective agent with numerous medicinal applications. EGCG effectively reduces tau and Aβ aggregation in ND models, promotes autophagy, and targets key signaling pathways like Nrf2-ARE, NF-κB, and MAPK. This review explores the molecular processes that underlie EGCG's neuroprotective properties, including its ability to regulate mitochondrial dysfunction, oxidative stress, neuroinflammation, and protein misfolding. Clinical research indicates that EGCG may enhance cognitive and motor abilities, potentially inhibiting disease progression despite absorption and dose optimization limitations. The substance has been proven to slow the amyloidogenic process, prevent protein aggregation, decrease amyloid cytotoxicity, inhibit fibrillogenesis, and restructure fibrils for synergistic therapeutic effects. The review highlights the potential of EGCG as a natural, multi-targeted strategy for NDs but emphasizes the need for further clinical trials to enhance its therapeutic efficacy.
诸如阿尔茨海默病、帕金森病、亨廷顿舞蹈症和肌萎缩侧索硬化症等神经退行性疾病,因其复杂的病理生理学和缺乏有效治疗方法而带来重大挑战。富含表没食子儿茶素没食子酸酯(EGCG)多酚成分的绿茶,已展现出作为一种具有多种药用价值的神经保护剂的潜力。EGCG能有效减少神经退行性疾病模型中的tau蛋白和β淀粉样蛋白(Aβ)聚集,促进自噬,并作用于如Nrf2-ARE、NF-κB和MAPK等关键信号通路。本综述探讨了EGCG神经保护特性背后的分子机制,包括其调节线粒体功能障碍、氧化应激、神经炎症和蛋白质错误折叠的能力。临床研究表明,尽管存在吸收和剂量优化方面的限制,但EGCG可能增强认知和运动能力,从而潜在地抑制疾病进展。该物质已被证明能减缓淀粉样蛋白生成过程、防止蛋白质聚集、降低淀粉样蛋白细胞毒性、抑制纤维形成,并重构纤维以产生协同治疗效果。本综述强调了EGCG作为神经退行性疾病天然多靶点治疗策略的潜力,但也强调需要进一步开展临床试验以提高其治疗效果。