氟喹诺酮类药物致神经系统和软骨毒性的机制研究进展  

Recent advances in the study of mechanisms of neurotoxicity and chondrotoxicity caused by fluoroquinolones

作　　者：俞春红[1] 潘任桃[1] 孙志良[1] 刘兆颖[1] 

机构地区：[1]湖南农业大学动物医学院,湖南省兽药工程技术研究中心,长沙410128

出　　处：《中国抗生素杂志》2013年第11期810-814,共5页Chinese Journal of Antibiotics

基　　金：氟喹诺酮类药物达氟沙星致猪肾小管上皮细胞损伤的分子机制研究(31101859)

摘　　要：本文综述近年来国内外公开发表的相关文献,总结分析氟喹诺酮类药物(FQs)致中枢神经不良反应和软骨毒性的分子机制。研究表明FQs产生的神经毒性与NMDA、GABA受体相关;其软骨毒性与细胞基质、DNA、Mg2+及β1整合素的影响有关。并证明FQs的毒性与氧化应激有密切关系,一些抗氧化剂和抗氧化酶能降低FQs的毒副作用。这为进一步深入研究氧化应激诱导FQs毒性机理提供了重要的理论指导,同时对临床合理用药来减少不良反应具有重要的意义。This paper reviewed many literatures which researched the toxicity of fluoroquinolones（FQs） in recent years.The mechanism of neurotoxicity and chondrotoxicity induced by fluoroquinolones was summarized. Results have indicated that the neurotoxicity of the fluoroquinolones is related to the NMDA and GABA receptor, and the chondrotoxicity is associated with cell matrix, DNA, Mg2＋ and integrin 131. In addition, the oxidative stress plays a crucial role in the the toxicity of FQs. Some antioxidants and antioxidant enzymes can reduce their side effect. These results can provide some theoretical guidance for the deep investigation on the relationship between oxidative stress and the toxicity of FQs, and also have an important significance for reducing the adverse reaction through rational medication in clinical.

关 键 词：氟喹诺酮类药物 神经系统不良反应 软骨毒性 氧化应激 

分 类 号：R978[医药卫生—药品]