Peripheral nerve injury constitutes a complex neurotraumatic pathology characterized by mechanical disruption of neural integrity, manifesting as multimodal sensorimotor deficits and impaired neuromuscular coordination. The primary clinical interventions include surgical tension-free suturing of the severed nerve ends and autologous nerve transplantation. Despite these interventions, patients often experience complications, and the outcomes are not entirely satisfactory for either patients or clinicians. Mesenchymal stem cells (MSCs) have gradually become a novel therapeutic option, with burgeoning preclinical evidence elucidating their multimodal therapeutic potential in peripheral nerve reconstruction. This research has produced promising outcomes, contributing to both fundamental research and translational medicine. However, a comprehensive synthesis of the roles of MSCs and their derivatives in nerve regeneration is still lacking. This article presents a review of the current research advancements in this area, aiming to encourage further investigations and therapeutic applications of MSCs and their derivatives in peripheral nerve injury and regenerative medicine.

Oxidative stress leads to chondrocyte apoptosis and extracellular matrix (ECM) degradation, thus contributing to the pathogenesis of osteoarthritis (OA). Herein, curcumin with remarkable antioxidant and anti-inflammatory activities has been employed as an organic ligand to coordinate ferric ions for enhancing the water-solubility and biocompatibility of natural product curcumin. The obtained iron-curcumin-based coordination nanoparticles (Fe-Cur NPs) exhibit great water-solubility and efficient reactive oxygen/nitrogen species (ROS/RNS) scavenging ability. In vitro chondrocyte evaluation experiments indicated that the intracellular ROS/RNS induced by interleukin 1β (IL-1β) could be efficiently scavenged by these Fe-Cur NPs and oxidative-stress-induced cell death could be preserved as well. In addition, post intra-articular (i.a.) injection into OA rat joints, Fe-Cur NPs could greatly inhibit OA progression via activating the nuclear factor-erythroid 2 related factor-2 (Nrf2) and inhibiting nod-like receptor protein-3 (NLRP3) inflammasome activation in primary rat chondrocytes, as well as decrease the production of matrix degrading proteases and other inflammatory mediators. The efficient antioxidation and anti-inflammation performance of Fe-Cur NPs endow them as a promising nanoplatform for treatment of various inflammatory diseases, and more detailed researches will be conducted in the future.