摘要
骨关节炎(osteoarthritis,OA)是一种关节软骨的退行性病变,以局限性、进行性关节软骨破坏及关节边缘骨赘形成为主,常伴有不同程度的滑膜炎症。迄今为止,OA的关节软骨损伤发病机制尚不明确,越来越多的研究发现氧化应激在其中起着重要作用。氧化应激所产生的活性氧自由基与氮自由基可致软骨细胞凋亡、软骨细胞外基质降解等。为此,本文综述了氧化应激诱导关节软骨损伤分子机理的进展,以推进OA病因发病机制与防治的深入研究。
Osteoarthritis （OA） is a degenerative disease of articular cartilage,which features local and progressive destruction of articular cartilage and osteophyte formation in the sub-cartilage edges, often accompanied with different degrees of synovial inflammation. The pathogenesis of articular cartilage injury of OA is still unclear up to now,and a growing number of studies have found that oxidative stress plays an important role in its pathogenesis. Reactive oxygen species and reactive nitrogen species produced by oxidative stress can cause apoptosis of chondrocytes and extracellular matrix degradation. This paper will focus on the molecular mechanism of articular cartilage injury induced by oxidative stress in order to promote an in-depth study for the etiology,pathogenesis and prevention of OA.
出处
《国外医学（医学地理分册）》
CAS
2013年第3期151-153,183,共4页
Foreign Medical Sciences：Section of Medgeography
基金
国家自然科学基金资助项目(No.81202157)
中央高校基本科研业务费专项资金资助
关键词
氧化应激
关节软骨
活性氧自由基
氮自由基
oxidative stress
articular cartilage
reactive oxygen species
reactive nitrogen species
