Peripheral neuropathies are prevalent disorders with limited therapies, where unresolved inflammation drives neuropathic pain. This project explores strategies combining pharmacological modulation of PPARγ with cellular and acellular nanoplatforms. In a sciatic nerve crush model, bone marrow multipotent cells (BMMC) migrated to the injury site within 24 h, a process inhibited by indomethacin. Indomethacin also reduced PGE₂ and increased PGJ₂, an endogenous PPARγ ligand, highlighting its regulatory role. Molecular analyses revealed that injury induced the expression of COX-1 and PPARγ, which was sustained by BMMC transplantation, whereas rosiglitazone did not significantly alter PPARγ expression. PLGA nanocapsules carrying rosiglitazone, with or without magnetic nanoparticles, were synthesized and are being optimized for stability and compatibility. Extracellular vesicles (EVs) from adipose-derived multipotent cells, functionalized with magnetic nanoparticles, were preliminarily validated for neuronal uptake without cytotoxicity. Behavioral assays showed partial pain relief with rosiglitazone and additive effects with BMMC. Altogether, results suggest PPARγ as a therapeutic target and the potential of bio-nanotechnological strategies to enhance regeneration and manage neuropathic pain in peripheral nerve injury.