Amniotic fluid stem cell conditioned medium's role in Schwann cell proliferation, survival, and cellular antioxidant activity under normative and oxidative stress conditions.

BACKGROUND: Peripheral nerve injuries present a major clinical challenge due to their high morbidity and often incomplete recovery of function. While autografts remain the gold standard for nerve repair, their use is constrained by limited donor availability and donor site complications. Alternative strategies, such as allografts and tissue-engineered grafts, have been developed but are still associated with suboptimal outcomes, including chronic pain and sensory disturbances. Thus, there is a need for novel therapies that can enhance nerve regeneration. Amniotic fluid stem cell conditioned medium (AFS-CM) houses regenerative properties that may be useful in peripheral nerve injury. This study aims to assess the role of AFS-CM on Schwann cell survival and proliferation under normative and oxidative stress conditions, preventing oxidative stress-induced premature senescence of Schwann cells in vitro and maintaining cellular redox homeostasis. METHODS: Primary Schwann cells were treated with various concentrations of AFS-CM. Cell proliferation was assessed using the Cell Counting Kit-8 (CCK-8) assay, and viability under oxidative stress was measured after exposing cells to hydrogen peroxide (H(2)O(2)). Reactive oxygen species (ROS) levels and both catalase and superoxide dismutase (SOD) levels were evaluated. Cellular senescence markers were also assessed to determine AFS-CM's protective effects. RESULTS: AFS-CM treatment resulted in a dose-dependent increase in Schwann cell proliferation (P<0.05). Under oxidative stress conditions, AFS-CM significantly improved cell viability compared to controls (P<0.05). ROS levels were markedly reduced in AFS-CM-treated cells (P<0.05), and this was accompanied by upregulation of catalase and SOD expression (P<0.05). Moreover, AFS-CM reduced stress-induced cellular senescence, as indicated by decreased senescence-associated β-galactosidase activity and lower expression of senescence markers (P<0.05). CONCLUSIONS: AFS-CM enhances Schwann cell proliferation, viability, and resistance to oxidative stress, while reducing cellular senescence. These findings suggest that AFS-CM could be a promising adjunctive therapy for peripheral nerve injuries by promoting Schwann cell resilience and regenerative capacity. Future studies are needed to validate these in vitro results in vivo and explore their potential clinical application for improving functional recovery in patients with peripheral nerve damage.