Fig. 6
Mst1 inhibition activated the autophagy/Keap1/Nrf2 signaling pathway in mBM-MSC exposed to H2O2. mBM-MSC/sh-Mst1 was transfected with siCTL-siRNA, siKeap1, or siNrf2; Mst1, Keap1, and Nrf2 expression levels in mBM-MSCs/sh-Mst1 were determined by Western blot analysis (a, **p < 0.01 vs. sh-Mst1 groups, #p > 0.05 vs. sh-Mst1 groups), pretreated with3-MA, and treated with 250 μM of H2O2 for 12 h. Cell apoptosis was detected by PI staining and pro caspase 3 expression analysis (b and c, **p < 0.01, #p > 0.05), LC3B and p62 expression in mBM-MSCs/sh-Mst1 and mBM-MSCs/sh-Mst1 + 3-MA (d, #p > 0.05 vs. H2O2 + sh-Mst1 groups, &p > 0.05 vs. H2O2 + sh-Mst1 + 3-MA groups). β-actin was used as the loading control. Data were expressed as mean ± SD