王佳薇¹ 何 迅^1,2

1.西南医科大学附属医院皮肤科 2.四川省人民医院皮肤科

摘要(Abstract)：

斑秃（AA）是一种自身免疫性毛发疾病，氧化应激在其发病中的作用日益受到关注。本文系统梳理近十余年相关文献，从临床证据、生物标志物、分子机制及治疗干预等方面进行综述。临床研究证实，AA患者存在氧化抗氧化失衡，丙二醛（MDA）、缺血修饰白蛋白（IMA）等氧化损伤标志物升高，超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、总抗氧化能力等指标降低，且与疾病活动性相关。新型标志物如IMA、一氧化氮合酶（NOS）、铁死亡相关基因显示出辅助诊断潜力。机制研究揭示，氧化应激可通过破坏毛囊免疫豁免（HF-IP）、诱导线粒体功能障碍、调控自噬与炎症小体活化、激活核因子E2相关因子2（Nrf2）及Janus激酶-信号转导与转录激活子（JAK-STAT）等通路参与发病，并与遗传、肠道微生态、心理因素交互作用。治疗方面，天然产物、纳米材料、活性氧（ROS）响应性递送系统及益生菌策略展现出前景。当前存在检测方法不统一、临床转化滞后等问题，未来需推进前瞻性队列研究、多组学技术应用及标志物标准化，为精准诊疗提供新思路。

关键词(KeyWords)：

斑秃；氧化应激；发病机制

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