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Physical Activity Prevents Cartilage Degradation: A Metabolomics Study Pinpoints the Involvement of Vitamin B6

机译:体力活动可防止软骨退化:一项代谢组学研究明确了维生素B6的参与

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摘要

Osteoarthritis (OA) is predominantly characterized by the progressive degradation of articular cartilage, the connective tissue produced by chondrocytes, due to an imbalance between anabolic and catabolic processes. In addition, physical activity (PA) is recognized as an important tool for counteracting OA. To evaluate PA effects on the chondrocyte lineage, we analyzed the expression of SOX9, COL2A1, and COMP in circulating progenitor cells following a half marathon (HM) performance. Therefore, we studied in-depth the involvement of metabolites affecting chondrocyte lineage, and we compared the metabolomic profile associated with PA by analyzing runners’ sera before and after HM performance. Interestingly, this study highlighted that metabolites involved in vitamin B6 salvage, such as pyridoxal 5′-phosphate and pyridoxamine 5′-phosphate, were highly modulated. To evaluate the effects of vitamin B6 in cartilage cells, we treated differentiated mesenchymal stem cells and the SW1353 chondrosarcoma cell line with vitamin B6 in the presence of IL1β, the inflammatory cytokine involved in OA. Our study describes, for the first time, the modulation of the vitamin B6 salvage pathway following PA and suggests a protective role of PA in OA through modulation of this pathway.
机译:骨关节炎(OA)的主要特征是由于合成代谢和分解代谢过程之间的失衡,软骨软骨(软骨细胞产生的结缔组织)逐渐退化。此外,体育锻炼(PA)被认为是抵抗OA的重要工具。为了评估PA对软骨细胞谱系的影响,我们分析了半马拉松(HM)运动后循环祖细胞中SOX9,COL2A1和COMP的表达。因此,我们深入研究了代谢物对软骨细胞谱系的影响,并通过分析HM运动前后运动员的血清来比较与PA相关的代谢组学特征。有趣的是,这项研究强调了参与维生素B6拯救的代谢产物,如吡ido醛5'-磷酸和吡ido胺5'-磷酸,受到高度调节。为了评估维生素B6在软骨细胞中的作用,我们在IL1β(涉及OA的炎性细胞因子)的存在下,用维生素B6处理了分化的间充质干细胞和SW1353软骨肉瘤细胞系。我们的研究首次描述了PA后维生素B6挽救途径的调节,并暗示了PA通过调节该途径在OA中的保护作用。

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