T-2毒素致大骨节病软骨损伤机制的研究进展  

Progress on the mechanism of cartilage damage induced by T-2 toxin in Kashin-Beck disease

作　　者：姚聪[1] 郝水楚 张纯[1] 董军[1] 贾雨萌 郭雄 Yao Cong;Hao Shuichu;Zhang Chun;Dong Jun;Jia Yumeng;Guo Xiong(The Second Affiliated Hospital of Xi'an Jiaotong University,Clinical Research Center for Endemic Disease Control of Shaanxi Province,Xi'an 710004,China;School of Public Health,Health Science Center,Xi'an Jiaotong University,Key Laboratory of Trace Elements and Endemic Diseases,National Health Commission of the People's Republic of China,Xi'an 710061,China)

机构地区：[1]西安交通大学第二附属医院陕西省地方病临床医学研究中心,西安710004 [2]西安交通大学医学部公共卫生学院,国家卫健委微量元素与地方病研究重点实验室,西安710061

出　　处：《中华地方病学杂志》2024年第5期421-424,共4页Chinese Journal of Endemiology

基　　金：国家自然科学基金国际合作重点项目(81620108026)

摘　　要：大骨节病(Kashin-Beck disease,KBD)是一种地方性、变形性骨关节病,可对发育过程中的四肢软骨内化骨造成损伤,病因至今尚未明确。近年来,国内外学者从免疫毒性与氧化应激、炎症反应、线粒体凋亡等方面研究了T-2毒素及其代谢物致大骨节病软骨损伤的机制,主要包括转化生长因子-β受体(TGF-βRs)信号通路、免疫调节因子、炎症因子白细胞介素(IL)-1β和凋亡酶激活因子(APAF1)等,它们通过诱导人体软骨细胞损伤、抑制基质合成和加速细胞分解代谢等方式促进KBD病程进展。本文从分子层面综述了T-2毒素的免疫毒性及其毒性作用与KBD软骨损伤关系的研究进展,以期为防治KBD提供科学依据。Kashin-Beck disease(KBD)is an endemic and degenerative osteoarthropathy that can cause damage to the endochondral ossification of the limbs during development.The etiology is still unclear.In recent years,scholars at home and abroad have studied the mechanism of T-2 toxin and its metabolites causing KBD cartilage damage from the perspectives of immunotoxicity,oxidative stress,inflammatory response,cell apoptosis,etc.,mainly including transforming growth factor-βreceptor(TGF-βRs)signaling pathway,immune regulatory factor,inflammatory factor IL-1βand apoptosis enzyme activating factor 1(APAF1),which promote the progression of KBD by inducing human chondrocyte injury,inhibiting matrix synthesis and accelerating cellular catabolism.This article reviews the research progress on the immunotoxicity of T-2 toxin and its toxic effects on KBD cartilage injury at the molecular level,in order to provide a scientific basis for prevention and treatment of KBD.

关 键 词：T-2毒素 免疫毒性 细胞凋亡 氧化应激 大骨节病 

分 类 号：R684.1[医药卫生—骨科学]