Salicin inhirits AGE-induced degradation of type II collagen and aggrecan in human SW1353 chondrocytes: therapeutic potential in osteoarthritis
Salicin inhirits AGE-induced degradation of type II collagen and aggrecan in human SW1353 chondrocytes: therapeutic potential in osteoarthritis
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DOI：
10.1080/21691401.2019.1591427
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发表时间：
2019-01-01
影响因子：
5.8
通讯作者：
Zhang, Shanyong
中科院分区：
文献类型：
--
作者：
Gao, Feng;Zhang, Shanyong
骨关节炎（OA）是一种主要的年龄相关性疾病，可能与晚期糖基化终产物（AGEs）的积累有关。AGEs诱导的基质金属蛋白酶（MMPs）和具有血小板反应蛋白1型基序的去整合素和金属蛋白酶（ADAMTS）过度降解II型胶原和聚集蛋白聚糖是骨关节炎发病机制中的关键事件。此外，核因子-κ B（NF-κ B）通路的激活诱导促炎细胞因子级联的表达，如白细胞介素（IL）-1 β和肿瘤坏死因子-α（TNF-α）。在本研究中，我们研究水杨苷，阿司匹林的主要成分之一，八角枫的衍生物，对AGE诱导的SW 1353人软骨细胞的关节细胞外基质的降解的影响。我们的研究结果揭示了水杨苷在挽救II型胶原蛋白和聚集蛋白聚糖的降解、减少氧化应激、减弱促炎细胞因子的表达和抑制AGEs刺激的软骨细胞中NF-κ B促炎信号通路的激活方面的新的有益作用。因此，水杨苷可能成为一种安全有效的治疗OA发展和进展的药物。
Osteoarthritis (OA) is a major age-related disease, which may be caused by the accumulation of advanced glycation end-products (AGEs). Excessive degradation of type II collagen and aggrecan by matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase with thrombospondin type 1 motif (ADAMTS) induced by AGEs is a pivotal event in the pathogenesis of osteoarthritis. In addition, activation of the nuclear factor-kappa B (NF-kappa B) pathway induces the expression of a cascade of proinflammatory cytokines, such as interleukin (IL)-1 beta and tumor necrosis factor-alpha (TNF-alpha). In the present study, we investigated the effects of salicin, one of the main constituents of aspirin and a derivative of Alangium chinense, on AGE-induced degradation of the articular extracellular matrix in SW1353 human chondrocytes. Our findings reveal a novel beneficial role of salicin in rescuing degradation of type II collagen and aggrecan, reducing oxidative stress, attenuating expression of proinflammatory cytokines, and inhibiting activation of the NF-kappa B proinflammatory signaling pathway in chondrocytes stimulated with AGEs. Salicin may thus have potential as a safe and effective therapy against the development and progression of OA.