伴鼻息肉的慢性鼻窦炎中的氧化应激：病理生理机制、生物标志物及治疗意义

文献信息

中文摘要

背景与目的： 伴鼻息肉的慢性鼻窦炎（CRSwNP）是一种异质性炎症性疾病，累及鼻窦黏膜，以持续症状、高复发率及对生活质量的显著影响为特征。越来越多的证据提示氧化应激在其病理生理中发挥作用，但其确切贡献仍未完全明确。材料与方法：按照SANRA建议开展了一项叙述性综述。使用PubMed、Scopus和Google Scholar进行结构化文献检索，以识别研究CRSwNP中氧化应激、抗氧化系统及分子通路的研究。纳入2000年1月至2026年3月发表的相关文章并进行批判性评价，区分临床证据与离体、体外及动物证据。结果：现有证据主要来自小型横断面病例对照研究，一致地将CRSwNP与氧化应激增加相关联，其特征为活性氧和活性氮水平升高、脂质过氧化产物及DNA损伤。抗氧化防御受损伴随这一失衡，尽管超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶等单个酶的结果在不同样本类型和检测方法间并不一致。在分子层面，氧化应激激活促炎信号通路，包括NF-κB和NLRP3炎症小体，并与上皮屏障功能障碍及2型免疫反应相关。氧化特征在嗜酸性与非嗜酸性内型之间似乎存在差异。此外，氧化应激是CRSwNP、哮喘和过敏性鼻炎之间合理的机制联系，支持“联合气道疾病”的概念。抗氧化策略几乎仅由临床前数据支持。结论：氧化应激是CRSwNP的一致特征，并且基于实验数据，可能是慢性炎症的放大器；然而，其在人类中的因果作用尚未确立。在氧化还原靶向策略能够整合入临床实践之前，需要标准化的、内型特异性的氧化生物标志物、纵向研究及随机试验。

英文摘要

Background and Objectives: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a heterogeneous inflammatory disease of the sinonasal mucosa characterized by persistent symptoms, high recurrence rates, and a significant impact on quality of life. Increasing evidence suggests that oxidative stress plays a role in its pathophysiology, although its precise contribution remains incompletely defined. Materials and Methods: A narrative review was conducted following SANRA recommendations. A structured literature search was performed using PubMed, Scopus, and Google Scholar to identify studies investigating oxidative stress, antioxidant systems, and molecular pathways in CRSwNP. Relevant articles published between January 2000 and March 2026 were included and critically appraised, distinguishing clinical from ex vivo, in vitro, and animal evidence. Results: Available evidence, derived mainly from small cross-sectional case-control studies, consistently associates CRSwNP with increased oxidative stress, characterized by elevated levels of reactive oxygen and nitrogen species, lipid peroxidation products, and DNA damage. Impaired antioxidant defenses accompany this imbalance, although findings for individual enzymes such as superoxide dismutase, catalase, and glutathione peroxidase are inconsistent across sample types and assays. At the molecular level, oxidative stress activates pro-inflammatory signalling pathways, including NF-κB and the NLRP3 inflammasome, and is linked to epithelial barrier dysfunction and type 2 immune responses. Oxidative signatures appear to differ between eosinophilic and non-eosinophilic endotypes. Furthermore, oxidative stress represents a plausible mechanistic link between CRSwNP, asthma, and allergic rhinitis, supporting the concept of united airways disease. Antioxidant strategies are supported almost exclusively by preclinical data. Conclusions: Oxidative stress is a consistent feature of CRSwNP and, on the basis of experimental data, a likely amplifier of chronic inflammation; however, a causal role in humans has not been established. Standardized, endotype-specific oxidative biomarkers, longitudinal studies, and randomized trials are needed before redox-targeted strategies can be integrated into clinical practice.