Fig. 3.

HGF secreted from hUC-MSCs promoted the activation of the PI3K-AKT pathway. A. Western blot showing the expression of p-AKT in mouse ovaries after 4 days of in vitro culture. The ability of the hUC-MSC-sec to increase the phosphorylation of AKT was greatly inhibited by the addition of HGF^ab. The expression of p-AKT was significantly increased in the HGF-treated group compared to controls. B. Immunofluorescence analysis showing the location of FOXO3a in mouse ovaries after 4 days of culture. The ability of the hUC-MSC-sec to promote FOXO3a cytoplasmic translocation was inhibited by the addition of HGF^ab. The arrowheads indicate the nuclear localization of FOXO3a, and the arrows indicate the cytoplasmic localization of FOXO3a. C. The proportion of CL-FOXO3a was significantly decreased in hUC-MSC-sec plus HGF^ab-treated ovaries (32.8 ± 4.6%) compared to the hUC-MSC-sec group (47.3 ± 7.7%). The proportion of CL-FOXO3a was significantly increased in HGF-treated ovaries (50.9 ± 3.1%), which was similar to the hUC-MSC-sec group, compared to controls (32.8 ± 3.5%). Data are shown as the mean ± SD, n = 6. ^**P < 0.01, and ^***P < 0.001. Scale bars, 100 μm