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Hyaluronic acid fragments enhance the inflammatory and catabolic response in human intervertebral disc cells through modulation of toll-like receptor 2 signalling pathways

机译:透明质酸片段通过调节toll样受体2信号通路增强人椎间盘细胞的炎症和分解代谢反应

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摘要

IntroductionIntervertebral disc (IVD) degeneration is characterized by extracellular matrix breakdown and is considered to be a primary cause of discogenic back pain. Although increases in pro-inflammatory cytokine levels within degenerating discs are associated with discogenic back pain, the mechanisms leading to their overproduction have not yet been elucidated. As fragmentation of matrix components occurs during IVD degeneration, we assessed the potential involvement of hyaluronic acid fragments (fHAs) in the induction of inflammatory and catabolic mediators.
机译:简介椎间盘退变(IVD)的特征在于细胞外基质分解,被认为是椎间盘源性背痛的主要原因。尽管椎间盘退变中促炎性细胞因子水平的升高与椎间盘源性背痛有关,但尚未阐明导致其过度生产的机制。由于IVD变性过程中发生了基质成分的断裂,因此我们评估了透明质酸片段(fHA)在诱导炎症和分解代谢介质中的潜在作用。

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