Peripheral blood mesenchymal stem cells repair oxidative damage and apoptosis in an H(2)O(2)-induced vitiligo oxidative stress in vitro model via the IL-10-mediated PI3K/AKT pathway.

Peripheral blood mesenchymal stem cells (PBMSCs) are a less invasive and more accessible source of adult multipotent stem cells than bone marrow mesenchymal stem cells (BMMSCs), because their collection does not involve anaesthesia and the risk of complications. In the present study, we observed that PBMSCs alone exhibited a higher concentration of IL-10 in the supernatant when cultured independently. Furthermore, the supernatant from the Transwell co-culture system of PBMSCs with H(2)O(2)-induced oxidative stress in B16 melanoma cells, which serves as an in vitro model for vitiligo, demonstrated elevated levels of IL-10. Western blot analysis revealed that the PI3K/AKT signaling pathway was activated in B16 melanoma cells, as evidenced by increased phosphorylation of AKT, enhanced expression of the antioxidant enzyme HO-1 and the anti-apoptotic protein Bcl-2, alongside decreased expression of the pro-apoptotic proteins Bax and Cleaved-Caspase 3. Notably, these effects were inhibited by the IL-10 neutralizing antibody (AB9969) and the PI3K inhibitor (LY294002). Collectively, our findings suggest that PBMSCs may mitigate oxidative damage and apoptosis in B16 melanoma cells through the paracrine activation of the PI3K/AKT signaling pathway by IL-10. This approach offers a novel, readily available, and minimally invasive cellular therapeutic strategy for vitiligo while also providing a theoretical basis for targeting antioxidant pathways in treatment.