Controlled-release curcumin attenuates progression of tendon ectopic calcification by regulating the differentiation of tendon stem/progenitor cells

Controlled-release curcumin attenuates progression of tendon ectopic calcification by regulating the differentiation of tendon stem/progenitor cells
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控释姜黄素通过调节肌腱干/祖细胞的分化来减轻肌腱异位钙化的进展

DOI:
10.1016/j.msec.2019.04.090
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发表时间:
2019-10-01
影响因子:
7.9
通讯作者:
Yin, Zi
Yin, Zi
中科院分区:
工程技术1区
文献类型:
--
作者:
Chen, Yangwu;Xie, Yubin;Yin, Zi

文献摘要

被引文献

相似文献

肌腱钙化是一个常见但棘手的问题,当损伤或肌腱病进展到晚期时,会导致疼痛和活动受限。这是因为肌腱干/祖细胞(TSPC)在炎症条件下可以进行异常的成骨分化。本研究旨在探讨天然抗炎药姜黄素在肌腱钙化中对TSPC分化的调节作用。在炎症刺激下,TSPC表现出更高的碱性磷酸酶活性和更频繁的矿化结节形成,这在培养体系中得到了验证;但姜黄素显著减轻了这些病理变化。在体内功能分析中,将壳聚糖微球包裹的姜黄素注射到大鼠肌腱异位钙化模型损伤部位。姜黄素组肌腱组织炎症明显减轻。控释姜黄素可部分挽救肌腱钙化,促进肌腱再生。本研究表明,控释姜黄素可调控TSPC的命运,在病理微环境中促进TSPC的肌腱形成和抑制TSPC的成骨,为肌腱疾病的治疗提供了一种新的策略。
Tendon calcification is a common but intractable problem leading to pain and activity limitation when injury or tendinopathy progresses into the late stage. This is because tendon stem/progenitor cells (TSPCs) can undergo aberrant osteogenic differentiation under inflammatory conditions. This study aims to investigate the effect of curcumin, a natural anti-inflammatory agent, on regulating the differentiation of TSPCs in tendon calcification. With inflammatory stimulation, TSPCs showed higher alkaline phosphatase activity and more frequent formation of mineralized nodules which were verified in the culture system; however, curcumin significantly alleviated these pathological changes. In in vivo function analysis, chitosan microsphere-encapsulated curcumin was delivered to injured sites of rat tendon ectopic calcification model. The inflammation in the tendon tissues of the curcumin group was significantly relieved. Controlled-release curcumin partially rescued tendon calcification and enhanced tendon regeneration in animal model. This study demonstrates that controlled-release curcumin can manipulate the fate decision of TSPCs, and that it promotes the tenogenesis and inhibits the osteogenesis of TSPCs in a pathological microenvironment, which provides a possible new therapeutic strategy for tendon disease.