PDF(Pubmed)
Abstract：
As the primary cause for chronic pain and disability in elderly individuals, osteoarthritis (OA) is one of the fastest-growing diseases due to the aging world population. To date, the impact of microenvironmental changes on the pathogenesis of OA remains poorly understood, greatly hindering the development of effective therapeutic approaches against OA. In this study, we profiled the differential metabolites in the synovial fluid from OA patients and identified the downregulation of vitamin B1 (VB1) as a metabolic feature in the OA microenvironment. In a murine destabilization of medial meniscus-induced OA model, supplementation of VB1 significantly mitigated the symptoms of OA. Cytokine array analysis revealed that VB1 treatment remarkably reduced the production of a pro-OA factor-C-C Motif Chemokine Ligand 2 (CCL2), in macrophages. Further evidence demonstrated that exogenous CCL2 counteracted the anti-OA function of VB1. Hence, our study unveils a unique biological function of VB1 and provides promising clues for the diet-based treatment of OA.
摘要：
作为老年人慢性疼痛和残疾的主要原因，骨关节炎（OA）是世界人口老龄化导致的增长最快的疾病之一。迄今为止,微环境变化对OA发病机制的影响尚不清楚，极大地阻碍了针对OA的有效治疗方法的发展。在这项研究中,我们对OA患者滑液中的差异代谢物进行了分析,并确定了维生素B1(VB1)的下调是OA微环境中的代谢特征.在小鼠内侧半月板诱导的OA模型的失稳中，补充VB1可显着减轻OA的症状。细胞因子阵列分析显示，VB1处理显着降低了pro-OA因子-C-C基序趋化因子配体2（CCL2）的产生，在巨噬细胞中。进一步的证据表明，外源性CCL2抵消了VB1的抗OA功能。因此，我们的研究揭示了VB1的独特生物学功能,并为基于饮食的OA治疗提供了有希望的线索.
