【摘要】 目的 了解USP49对IL-1β诱导的软骨细胞凋亡及细胞外基质降解的影响。方法 首先基于数据库了解USP49在骨关节炎患者中的表达水平。原代培养软骨细胞并鉴定，使用不同浓度的IL-1β预处理软骨细胞，检测USP49基因表达与蛋白水平后，选择合适的IL-1β浓度模拟骨关节炎。使用IL-1β处理构建的USP49过表达软骨细胞，检测软骨细胞凋亡，测定USP49、β-catenin及软骨降解相关蛋白MMP-1、MMP-13表达。结果 较正常人样本，USP49在骨性关节炎患者中表达显著降低。原代软骨细胞经不同浓度IL-1β预处理后，USP49表达明显抑制，且随浓度增加，抑制作用增强。USP49过表达可显著减弱IL-1β诱导的细胞凋亡，抑制β-catenin、MMP-1、MMP-13表达。结论 USP49可能通过Wnt/β-catenin通路抑制软骨细胞凋亡及细胞外基质降解，减轻IL-1β诱导的软骨退变。更多还原

【Abstract】 Objective To investigate the effect of USP49 on chondrocyte apoptosis and expression of proteins related to cartilage metabolism induced by IL-1β. Methods The expression of USP49 in osteoarthritis patients was determined based on GSE57218 database. Primary Rat articular chondrocytes were cultured and identified. After being pretreated with different concentrations of IL-1β respectively, USP49 gene expression was detected to selecting appropriate IL-1β concentration for simulating osteoarthritis. After incubation with 10 ng/ml IL-1β, the apoptosis of constructed USP49 overexpressed chondrocyte and the expression of β-catenin, proteins related to cartilage degradation were detected. Results The expression of USP49 was significantly decreased in patients with osteoarthritis. RT-PCR and Western blot showed that IL-1β significantly inhibited USP49 expression in a concentration-dependent manner. Over-expressioned USP49 significantly attenuated the apoptosis of chondrocytes induced by IL-1β, inhibited Wnt/β-catenin pathway and the expression of proteins related to cartilage degradation. Conclusion USP49 inhibits chondrocyte apoptosis and alleviates cartilage degradation induced by IL-1β through Wnt/β-catenin pathway.更多还原