NETs介导中药和天然产物靶向治疗炎症性肠病研究进展

Research progress on NETs mediated targeted treatment of inflammatory bowel disease with traditional Chinese medicine and natural products

关键词:  炎症性肠病  中药  天然产物  中性粒细胞胞外诱捕网  炎症

Key words:  inflammatory bowel disease  traditional Chinese medicine  natural products  neutrophil extracellular trapping net  inflammation

摘要:

炎症性肠病（IBD）是一种自身免疫性疾病，包括溃疡性结肠炎和克罗恩病。中性粒细胞在先天免疫中发挥关键作用，能够迁移至炎症部位，通过吞噬病原体、释放活性氧（ROS）介导氧化应激，并形成中性粒细胞胞外诱捕网（NETs），从而协同促进炎症反应。NETs是富含生物活性蛋白的DNA网络，它们的过度释放会加剧炎症，破坏肠道屏障，损害血管内皮细胞，并增加IBD血栓形成的风险。尽管IBD的病因尚不清楚，但失调的NETs释放与肠道炎症的发展密切相关。鉴于常规IBD药物疗效有限或不良反应明显，传统中药和天然产品有希望成为潜在替代常规治疗的选择。文章综述了NETs对于IBD的影响，并总结了中药和天然产物靶向NETs治疗包括IBD在内的炎症类疾病的临床前研究。通过阐明其机制，旨在支持未来中药和天然产物的临床转化。

Abstract:

Inflammatory bowel disease(IBD) is an autoimmune condition encompassing ulcerative colitis and Crohn's disease. Neutrophils play a pivotal role in innate immunity by migrating to inflammatory sites, where they phagocytize pathogens, induce oxidative stress through the release of reactive oxygen species(ROS), and form neutrophil extracellular traps(NETs), collectively amplifying the inflammatory response. NETs are DNA-based networks rich in bioactive proteins, and their excessive release exacerbates inflammation, disrupts the intestinal barrier, damages vascular endothelial cells, and increases the risk of thrombosis in IBD. Although the etiology of IBD remains unclear, dysregulated NETs formation is closely linked to the progression of intestinal inflammation. Given the limited efficacy or significant side effects of conventional IBD medications, traditional Chinese medicine and natural products offer promising potential as alternatives to standard treatments. This review explores the impact of NETs on IBD and summarizes preclinical studies on translation of traditional Chinese medicine and natural products targeting NETs for treating inflammatory diseases, including IBD. By elucidating the underlying mechanisms, we aim to support the future clinical translation of traditional Chinese medicine and natural products.