Inhibition of ROS activity by controlled release of proanthocyanidins from mesoporous silica nanocomposites effectively ameliorates heterotopic ossification in tendon
Inhibition of ROS activity by controlled release of proanthocyanidins from mesoporous silica nanocomposites effectively ameliorates heterotopic ossification in tendon
复制标题
通过介孔二氧化硅纳米复合材料控制释放原花青素来抑制 ROS 活性，有效改善肌腱异位骨化
DOI：
10.1016/j.cej.2021.129415
复制
发表时间：
2021-04-24
影响因子：
15.1
通讯作者：
Yin, Zi
中科院分区：
文献类型：
--
作者：
Liu, Richun;Zhou, Bo;Yin, Zi
在肌腱病的炎症环境中，肌腱干/祖细胞（TSPC）已被证明异常分化为骨软骨谱系，导致肌腱晚期异位骨化（HO），从而严重损害组织功能并使患者的活动恶化。然而，由于TSPC异常分化的机制尚不清楚，目前尚无有效的肌腱病治疗方法。在这篇文章中，在肌腱病样本中发现了高水平的活性氧（ROS）。体外结果表明，原花青素（PC）可以通过清除过量的 ROS 来潜在地调节 TSPC 的分化，从而促进肌腱形成而不是软骨形成或成骨。此外，体内结果表明，负载PC的介孔二氧化硅纳米复合材料（MSNs-PC）通过抑制氧化应激，阻碍修复肌腱中H2O的复发，表现出抗炎作用。我们的研究结果表明，肌腱病中的 ROS 水平很高，这可能是 TSPC 异常分化的原因。 MSNs-PCs 可以通过清除过量的 ROS 来有效改善肌腱的 HO，为其他 ROS 相关疾病提供了一个有希望的途径。
In the inflammatory environment of tendinopathy, tendon stem/progenitor cells (TSPCs) have been demonstrated to aberrantly differentiate into osteochondral lineage causing late-stage heterotopic ossification (HO) of the tendon, which severely damages tissue function and worsens patients' activities. However, no effective treatment for tendinopathy currently exist because the mechanism underlying the TSPCs abnormal differentiation is unclear. In this article, high levels of reactive oxygen species (ROS) were found in tendinopathy samples. In vitro results revealed that proanthocyanidins (PC) can potentially regulate the differentiation of TSPCs by scavenging excess ROS, which would promote tenogenesis instead of chondrogenesis or osteogenesis. Moreover, in vivo results demonstrated that PC-loaded mesoporous silica nanocomposite (MSNs-PC) hinders the recurrence of HO in repaired tendons owing to the inhibition of oxidative stress, showing anti-inflammatory effects. Our findings indicate a high level of ROS in tendinopathy, which is probably the cause of aberrant differentiation of TSPCs. MSNs-PCs can effectively ameliorate HO of the tendon by scavenging excess ROS, providing a promising avenue to for other ROS-related diseases.