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慢性炎症是皮肤衰老进程中的关键驱动因素,其通过激活 MAPK、NF-κB 等关键信号通路,促进 IL-1β、TNF-α 等炎症因子的释放,在分子、细胞、器官及免疫学等多个层面协同加剧皮肤衰老的发生与发展。壳聚糖作为一种天然多糖,展现出显著的抗炎生物活性,其作用机制主要包括抑制 MAPK、PI3K/Akt 等信号通路的异常激活,减少 IL-6、TNF-α 等促炎因子的过度表达,并通过双向免疫调节作用平衡巨噬细胞功能。研究表明,壳聚糖及其衍生物不仅能直接干预炎症信号传导,还可增强巨噬细胞的吞噬能力以维持组织微环境稳态。O- 羧甲基壳聚糖作为壳聚糖的重要衍生物,通过 O 位羧甲基化修饰显著提升了其水溶性与生物相容性,同时兼具抗氧化、抗菌等生物学特性,为开发高效、安全的抗炎抗衰护肤产品提供了重要的应用前景。
Abstract:Chronic inflammation is a key driver in the process of skin aging. It synergistically exacerbates the occurrence and development of skin aging at multiple levels—molecular, cellular, organ, and immunological—by activating key signaling pathways such as MAPK and NF-κB and promoting the release of inflammatory factors including IL-1β and TNF-α. As a natural polysaccharide, chitosan exhibits significant anti-inflammatory biological activity. Its mechanisms of action mainly involve inhibiting the abnormal activation of signaling pathways like MAPK and PI3K/Akt, reducing the overexpression of pro-inflammatory factors such as IL-6 and TNF-α, and balancing macrophage function through bidirectional immunomodulatory effects. Studies have demonstrated that chitosan and its derivatives not only directly interfere with inflammatory signal transduction but also enhance the phagocytic capacity of macrophages to maintain tissue microenvironment homeostasis. As an important derivative of chitosan, O-carboxymethyl chitosan significantly improves its water solubility and biocompatibility via O-position carboxymethylation modification. It also possesses biological properties such as antioxidant and antibacterial activities, offering important application prospects for the development of efficient and safe anti-inflammatory and anti-aging skincare products.
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引用信息:
[1]阎凌翔,方庆秋 ,徐宇帆,等.皮肤炎性衰老的作用机制及壳聚糖与其 O 位羧甲基衍生物的干预路径探究[J],2026,3(02):27-35.