Fig. 2

rhMG53 lessens H₂O₂-induced oxidative injury to hUC-MSCs and promotes cell migration. a Representative images of hUC-MSCs with and without 200 μM H₂O₂ treatment. b Time- and dose-dependent effects of H₂O₂ on hUC-MSCs. Cells were cultured in 0, 50, 100, 200, 300, or 400 μM H₂O₂, and OD450 was measured at 0, 8, 16, 24, 32, and 40 h post-treatment. Two hundred micromolar H₂O₂ was used for subsequent experiments to induce hUC-MSC oxidative damage. c Dose-dependent effects of MG53 on hUC-MSCs. Thirty micrograms per milliliter of rhMG53 was chosen for our in vitro experiments. d rhMG53 facilitates hUC-MSC proliferation and protects against H₂O₂-induced injury. e Quantification of apoptosis rate from Annexin V-FITC/PI flow cytometry. f Apoptosis of hUC-MSCs was detected and analyzed by Annexin V-FITC and PI double staining and flow cytometry as well. g Cell senescence was evaluated using a SA-β-gal kit. Senescent cells were dyed blue. h Transwell assay was used to assess cell migration. Migrated cells were stained with CV. Scale bar = 100 μm. Quantification of cell senescence (i) and migration (j). SOD activity (k) and MDA content (l) were measured from hUC-MSC lysates. Data are presented as mean ± SEM. n = 6 per group. *p < 0.05, compared with CON group; ^#p < 0.05, compared with MG53 + H₂O₂ group