Fig. 8

Schematical representation of the protective mechanism of H₂O₂ preconditioning for improving the therapeutic potential of BMSCs. A low dose of H₂O₂ (50 μM) acts in the signaling pathways as a second messenger. H₂O₂ preconditioning-induced BMSC protection seems to involve augmenting the SDF-1/CXCR4 axis and activation of PI3K/Akt/mTOR and inhibiting GSK-3β activity, leading to enhancing abilities of BMSC proliferation, migration, angiogenesis, and anti-apoptosis. And the PI3K/Akt pathway is also one of the downstream pathways that activated the SDF-1/CXCR4 axis [9, 10, 18,19,20,21]. In addition, low-dose H₂O₂ directly activated this pathway through diffusion into the cytoplasm as a second messenger may be another activation pathway [17, 25]. The PI3K inhibitor (LY294002) could block the protective effect induced by 50 μM H₂O₂ preconditioning