Wang Tianzi, Shi Wenling, Mao Zijun, Xie Wei, Wan Guoqing
School of Chemistry and Chemical Engineering, Shanghai University of Engineering Science, Shanghai 201620, China.
School of Pharmacy, Shanghai University of Medicine and Health Sciences, Shanghai 201318, China.
Mar Drugs. 2025 Jun 30;23(7):274. doi: 10.3390/md23070274.
Alzheimer's disease (AD) is characterized by β-amyloid plaques, neurofibrillary tangles, neuroinflammation, and oxidative stress-pathological features that pose significant challenges for the development of therapeutic interventions. Given these challenges, this review comprehensively evaluates the neuroprotective mechanisms of bioactive compounds derived from , including polysaccharides and phycobiliproteins, which are considered a promising source of natural therapeutics for AD. constituents exhibit neuroprotective activities through multiple mechanisms. Sulfated polysaccharides (e.g., carrageenan, porphyran) suppress NF-κB-mediated neuroinflammation, modulate mitochondrial function, and enhance brain-derived neurotrophic factor (BDNF) expression. Phycobiliproteins (phycoerythrin, phycocyanin) and peptides derived from their degradation scavenge reactive oxygen species (ROS) and activate antioxidant pathways (e.g., Nrf2/HO-1), thus mitigating oxidative damage. Carotenoids (lutein, zeaxanthin) improve cognitive function through the inhibition of acetylcholinesterase and pro-inflammatory cytokines (TNF-α, IL-1β), while phenolic compounds (bromophenols, diphlorethol) provide protection by targeting multiple pathways involved in dopaminergic system modulation and Nrf2 pathway activation. Emerging extraction technologies-including microwave- and enzyme-assisted methods-have been shown to optimize the yield and maintain the bioactivity of these compounds. However, the precise identification of molecular targets and the standardization of extraction techniques remain critical research priorities. Overall, -derived compounds hold significant potential for multi-mechanism AD interventions, providing novel insights for the development of therapeutic strategies with low toxicity.
阿尔茨海默病(AD)的特征在于β-淀粉样蛋白斑块、神经原纤维缠结、神经炎症和氧化应激——这些病理特征对治疗干预措施的开发构成了重大挑战。鉴于这些挑战,本综述全面评估了源自[具体来源未给出]的生物活性化合物的神经保护机制,包括多糖和藻胆蛋白,它们被认为是AD天然治疗药物的一个有前景的来源。[具体来源未给出]的成分通过多种机制表现出神经保护活性。硫酸化多糖(如角叉菜胶、紫菜聚糖)抑制NF-κB介导的神经炎症,调节线粒体功能,并增强脑源性神经营养因子(BDNF)的表达。藻胆蛋白(藻红蛋白、藻蓝蛋白)及其降解产生的肽清除活性氧(ROS)并激活抗氧化途径(如Nrf2/HO-1),从而减轻氧化损伤。类胡萝卜素(叶黄素、玉米黄质)通过抑制乙酰胆碱酯酶和促炎细胞因子(TNF-α、IL-1β)来改善认知功能,而酚类化合物(溴酚、二羟基甲苯)通过靶向参与多巴胺能系统调节和Nrf2途径激活的多种途径提供保护。新兴的提取技术——包括微波辅助和酶辅助方法——已被证明可以优化这些化合物的产量并保持其生物活性。然而,分子靶点的精确识别和提取技术的标准化仍然是关键的研究重点。总体而言,源自[具体来源未给出]的化合物在多机制AD干预方面具有巨大潜力,为开发低毒性治疗策略提供了新的见解。