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硒纳米颗粒抑制肌腱源性干/祖细胞中的氧化应激并促进肌腱细胞标志物表达。

Selenium Nanoparticles Suppressed Oxidative Stress and Promoted Tenocyte Marker Expression in Tendon-Derived Stem/Progenitor Cells.

作者信息

Lui Pauline Po Yee, Huang Caihao, Zhang Xing

机构信息

Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong SAR, China.

Center for Neuromusculoskeletal Restorative Medicine Ltd., Hong Kong Science Park, Shatin, New Territories, Hong Kong SAR, China.

出版信息

Antioxidants (Basel). 2024 Dec 15;13(12):1536. doi: 10.3390/antiox13121536.

DOI:10.3390/antiox13121536
PMID:39765864
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11727164/
Abstract

Traumatic tendon injuries generate reactive oxygen species and inflammation, which may account for slow or poor healing outcomes. Selenium is an essential trace element presented in selenoproteins, many of which are strong antioxidant enzymes. Selenium nanoparticles (SeNPs) have been reported to promote tissue repair due to their anti-oxidative, anti-inflammatory, anti-apoptotic, and differentiation-modulating properties. However, its effects on the functions of tendon-derived stem/progenitor cells (TDSCs) and tendon healing have not been reported. This study examined the effects of SeNPs on the functions of hydroperoxide (HO)-stimulated TDSCs. Rat patellar TDSCs were treated with HO with or without SeNPs. The viability, marker of proliferation, oxidative stress, inflammation, apoptosis, and tenocyte marker expressions of HO-stimulated TDSCs after SeNPs treatment were assessed. Our results showed that SeNPs increased the viability and expression of the marker of proliferation of TDSCs exposed to HO, while concurrently reducing oxidative stress, inflammation, and apoptosis. Additionally, the expressions of tenocyte markers were significantly elevated in HO-treated TDSCs after treatment with SeNPs. Furthermore, the expressions of and also increased after SeNPs treatment in HO-stimulated TDSCs. In conclusion, SeNPs mitigated oxidative stress, inflammation, and apoptosis while enhancing the survival and expression of the marker of proliferation of TDSCs in an oxidative stress environment. Additionally, it promoted the fate of TDSCs towards the tenocyte lineage in the presence of such oxidative stress. The increased expressions of and likely mediated the anti-oxidative and anti-inflammatory effects of SeNPs. SeNPs hold promise as a novel intervention for promoting tendon healing.

摘要

创伤性肌腱损伤会产生活性氧和炎症,这可能是愈合缓慢或效果不佳的原因。硒是硒蛋白中的一种必需微量元素,其中许多是强大的抗氧化酶。据报道,硒纳米颗粒(SeNPs)因其抗氧化、抗炎、抗凋亡和调节分化的特性而能促进组织修复。然而,其对肌腱衍生的干/祖细胞(TDSCs)功能和肌腱愈合的影响尚未见报道。本研究考察了SeNPs对过氧化氢(HO)刺激的TDSCs功能的影响。将大鼠髌腱TDSCs用HO处理,同时或不添加SeNPs。评估了SeNPs处理后HO刺激的TDSCs的活力、增殖标志物、氧化应激、炎症、凋亡及肌腱细胞标志物表达。我们的结果表明,SeNPs提高了暴露于HO的TDSCs的活力和增殖标志物的表达,同时降低了氧化应激、炎症和凋亡。此外,在用SeNPs处理后,HO处理的TDSCs中肌腱细胞标志物的表达显著升高。此外,在HO刺激的TDSCs中,SeNPs处理后 和 的表达也增加。总之,SeNPs减轻了氧化应激、炎症和凋亡,同时在氧化应激环境中提高了TDSCs的存活率和增殖标志物的表达。此外,在这种氧化应激存在的情况下,它促进了TDSCs向肌腱细胞谱系的分化。 和 表达的增加可能介导了SeNPs的抗氧化和抗炎作用。SeNPs有望成为促进肌腱愈合的一种新型干预措施。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b9/11727164/5f39e699a57e/antioxidants-13-01536-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b9/11727164/a7210955c2e5/antioxidants-13-01536-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b9/11727164/c8cdf39a335b/antioxidants-13-01536-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b9/11727164/e91357252774/antioxidants-13-01536-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b9/11727164/7bb55f93d300/antioxidants-13-01536-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b9/11727164/6542e1982ce8/antioxidants-13-01536-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b9/11727164/ec5f7a5e4fd3/antioxidants-13-01536-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b9/11727164/5f39e699a57e/antioxidants-13-01536-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b9/11727164/a7210955c2e5/antioxidants-13-01536-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b9/11727164/c8cdf39a335b/antioxidants-13-01536-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b9/11727164/e91357252774/antioxidants-13-01536-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b9/11727164/7bb55f93d300/antioxidants-13-01536-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b9/11727164/6542e1982ce8/antioxidants-13-01536-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b9/11727164/ec5f7a5e4fd3/antioxidants-13-01536-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b9/11727164/5f39e699a57e/antioxidants-13-01536-g007.jpg

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