FIGURE 3.

CaM/CaMKII and Nrf2/HO‐1/NQO1 signaling pathways were attenuated after YWHAE knockdown. (a) Changes in 14‐3‐3ε, t‐Nrf2, n‐Nrf2, HO‐1, NQO1, CaM, p‐CaMKII, CaMKII, p16^INK4a, and p21 expression in hAMSCs upon different treatments. (b–i) Relative expression levels of 14‐3‐3ε, n‐Nrf2, t‐Nrf2, CaM, CaMKII, p‐CaMKII, HO‐1, NQO1, p16^INK4a, and p21. N = 3. N‐Nrf2, nuclear Nrf2; t‐Nrf2, total Nrf2; p‐CaMKII, phosphorylated CaMKII; control, control group; H₂O₂, senescent group; GA‐D, GA‐D treatment group; mock‐vehicle, GA‐D treatment group plus empty carrier; h‐14‐3‐3ε, GA‐D treatment group plus YWHAE overexpression; sh‐14‐3‐3ε, GA‐D treatment group plus YWHAE knockdown; $\overline{x}\pm \mathrm{SD}$, mean ± standard deviation. *p < 0.05, **p < 0.01. CaM, calmodulin; CaMKII, CaM‐dependent protein kinase II; GA‐D, ganoderic acid D; H₂O₂, hydrogen peroxide; hAMSC, human amniotic mesenchymal stem cell; Nrf2, nuclear erythroid 2‐related factor 2.