氧化应激介导绝经后骨质疏松发病机制的研究进展  

Research progress on the pathogenesis of oxidative stress mediated osteoporosis

作　　者：孙振双[1] 耿元卿[1] 张丽君 郭海英[1] 

机构地区：[1]南京中医药大学第二临床医学院,南京210023 [2]洛阳市第一中医院妇产科,洛阳471000

出　　处：《中国骨质疏松杂志》2016年第8期1063-1067,共5页Chinese Journal of Osteoporosis

基　　金：江苏省研究生科研创新计划项目(KYZZ15-0272)

摘　　要：研究证实氧化应激是绝经后骨质疏松症的重要发病机制。妇女绝经后受衰老和雌激素不足等因素的共同影响,体内氧化应激水平增高,使骨重建失衡,导致骨质疏松发病。其中衰老、雌激素缺乏、Fox O转录因子、Nox亚型与活性氧的产生和骨质疏松发病有着密切的关系。近年来,氧化应激导致骨质疏松发病机制方面的研究日益增多,并取得了一定进展,本文通过查阅国内外相关文献,对氧化应激介导绝经后骨质疏松发病机制的研究进展进行综述,总结了氧化应激导致绝经后骨质疏松发病的相关因素及机制,并结合抗氧化治疗骨质疏松的研究现状和远景提出了思考。Oxidative stress may play an important role in the pathogenesis of postmenopausal osteoporosis. After menopause,the body is affected by a combination of factors,including aging,estrogen deficiency,etc.,which increases the level of oxidative stress in the body. Oxidative stress can cause bone remodeling imbalance,and eventually can lead to osteoporosis. Of these,aging,estrogen deficiency,Fox O transcription factor and Nox subtype all have a close relationship with the production of reactive oxygen species and the pathogenesis of osteoporosis. In recent years,a number of studies investigated the pathogenesis of osteoporosis induced by oxidative stress, and progress has been made. By reviewing international and domestic literatures, this article summarizes the research progress on the pathogenesis of osteoporosis induced by oxidative stress. We also summarized the related factors and mechanisms of oxidative stress in the pathogenesis postmenopausal osteoporosis,and put forward some thoughts on the current research status and the perspectives of using antioxidant in the treatment of osteoporosis.

关 键 词：氧化应激 绝经 骨质疏松 氧自由基 

分 类 号：R589.5[医药卫生—内分泌]