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

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.