Porous Se@SiO2 nanoparticles improve oxidative injury to promote muscle regeneration via modulating mitochondria

Plain language summary Muscle injuries are very common in daily life and in sports. When a muscle is injured, the local response inhibits the regeneration and differentiation of stem cells inside the muscle, thus hindering muscle regeneration. The authors have recently developed a nanoparticle with the ability to protect muscle stem cell function, promote stem cell proliferation and differentiation and facilitate muscle regeneration after skeletal muscle injury in rats. Thus, this study reveals the potential of porous Se@SiO2 nanoparticles in skeletal muscle diseases associated with mitochondrial dysfunction. Background: Acute skeletal muscle injuries are common among physical or sports traumas. The excessive oxidative stress at the site of injury impairs muscle regeneration. The authors have recently developed porous Se@SiO2 nanoparticles (NPs) with antioxidant properties. Methods: The protective effects were evaluated by cell proliferation, myogenic differentiation and mitochondrial activity. Then, the therapeutic effect was investigated in a cardiotoxin-induced muscle injury rat model. Results: Porous Se@SiO2 NPs significantly protected the morphological and functional stability of mitochondria, thus protecting satellite cells from H2O2-induced damage to cell proliferation and myogenic differentiation. In the rat model, intervention with porous Se@SiO2 NPs promoted muscle regeneration. Conclusion: This study reveals the application potential of porous Se@SiO2 NPs in skeletal muscle diseases related to mitochondrial dysfunction.

Automated summary

Muscle injuries are common and hinder muscle regeneration. Researchers have developed porous Se@SiO2 nanoparticles that protect stem cell function, promote proliferation and differentiation, and facilitate muscle regeneration. This study reveals the potential application of porous Se@SiO2 nanoparticles in skeletal muscle diseases associated with mitochondrial dysfunction.