白介素-1β诱导关节软骨细胞凋亡的分子机理

The Molecular Mechanism of IL-1β-induced Articular Chondrocytes Apoptosis

骨关节炎(OA)是一种退行性病变,表现为局限性、进行性关节软骨破坏及关节边缘骨赘形成,并伴有不同程度的滑膜炎症。软骨细胞是成熟关节软骨中唯一的细胞类型,它负责细胞外基质的合成和更新,并维持基质的完整。目前OA的发病机制尚不明确,但越来越多的研究发现致炎细胞因子白细胞介素-1β(IL-1β)起着重要的作用。IL-1β能诱导软骨细胞凋亡,其机制有一氧化氮(NO)、活性氧(ROS)和丝裂原激活的蛋白激酶(MAPK)等途径。IL-1β也是OA病变进展中破坏软骨细胞代谢平衡的主要细胞因子之一。对IL-1β诱导关节软骨细胞凋亡的分子机理的深入研究,将有助于新药的研发和骨关节病的治疗。

Osteoarthritis（OA） is a degenerative disease.It shows local,progressive destruction of articular cartilage and joint marginal osteophyte formation,and is accompanied by varying degrees of synovitis.The chondrocytes,which is the only cell type present in mature cartilage,is responsible for the synthesis and update of extracellular matrix and the maintenance of matrix integrity.Although the pathogenesis of OA is not yet clear,an increasing number of studies have found that cytokine interleukin-1β（IL-1β） plays an important role.There are nitric oxide（NO）,reactive oxygen species（ROS）,mitogen-activated protein kinase（MAPK） pathways in IL-1β-induced chondrocytes apoptosis.IL-1βis also an major cytokine for destroying the balance of chondrocytes metabolism in OA progression.Advances in the understanding of the molecular mechanism of IL-1 P-induced articular chondrocytes apoptosis may contribute to the discovery of new drugs and the OA therapy.