氧化应激在系统性红斑狼疮发病机制中的作用  

The role of oxidative stress in the pathogenesis of systemic lupus erythematosus

作　　者：陈琴 夏育民[1] CHEN Qin;XIA Yumin(Department of Dermatology,the Second Affiliated Hospital of Xi’an Jiaotong University,Xi’an 710004,China)

机构地区：[1]西安交通大学第二附属医院皮肤科,西安710004

出　　处：《国际免疫学杂志》2024年第2期183-189,共7页International Journal of Immunology

基　　金：国家自然科学基金重点项目(81630081)。

摘　　要：系统性红斑狼疮(systemic lupus erythematosus,SLE)是一种多系统受累的自身免疫性疾病,通常认为遗传与免疫因素主要参与其发病。近年研究发现,氧化应激可导致SLE患者辅助性T细胞和调节性T细胞分化失衡以及线粒体功能障碍,通过对脂质、蛋白质和核酸等生物大分子进行氧化修饰,触发自身免疫,导致免疫复合物沉积并损伤靶器官。氧化应激还能降低DNA甲基化水平从而使相关基因过表达,但具体机制尚不清楚。抑制氧化应激可作为防治SLE的有效方法,延缓病情发展。文章将着重讨论氧化应激如何参与SLE的发生发展,以及针对氧化应激的抗氧化治疗方法,为SLE患者的临床治疗提供新的思路。Systemic lupus erythematosus(SLE)is a kind of autoimmunity disease with multiple systems involved.It is generally believed that genetic and immune factors are involved in the pathogenesis of SLE.In recent years,it was found that oxidative stress leads to the imbalance of helper T cell and regulatory T cell differentiation and mitochondrial dysfunction in SLE patients.Oxidative modification of lipids and proteins may trigger autoimmunity and lead to immune complex deposition and damage to target organs.Oxidative stress also reduces the level of DNA methylation and promotes the expression of related genes,but the exact mechanism is still unclear.The oxidative stress pathway may be used as a new target for the treatment of SLE patients,and alleviate the disease progression.The review will focus on how oxidative stress is involved in the pathogenesis of SLE and the antioxidant therapies,so as to provide new ideas for the clinical treatment of patients with SLE.

关 键 词：红斑狼疮 氧化应激 靶器官损害 抗氧化治疗 

分 类 号：R593.241[医药卫生—内科学]