Research Paper Volume 10, Issue 10 pp 2954—2972
Melatonin prevents senescence of canine adipose-derived mesenchymal stem cells through activating NRF2 and inhibiting ER stress
Figure 4. Melatonin attenuates senescence of cADMSCs through activating NRF2. (A) Relative levels of Nrf2, Ho-1, Gclc, and Nqo1 transcripts in melatonin-treated cADMSCs. (B) Dual-luciferase assay of melatonin-, ramelteon+melatonin-, and luzindole+melatonin-treated P11 cADMSCs. (C) Immunohistochemistry of NRF2 in control, melatonin-, ramelteon+melatonin- and luzindole+melatonin-treated P11 cADMSCs. bar = 200 μm (D) Western blot quantification of nucleoprotein and cytosolic proteins in melatonin-, ramelteon+melatonin- and luzindole+melatonin-treated cADMSCs, with oltipraz treatment as positive control. Oltipraz (15μM), an activator of NRF2, was used as the positive control. (E) Expression of Nrf2 and its target genes in P3 negative control, mock, vector, shNrf2-1, and shNrf2-2 cADMSCs. (F) Doubling time of P3 negative control, mock, vector and shNrf2-1 cADMSCs. (G) SA-β-gal S of P3 negative control, mock, vector and shNrf2-1 cADMSCs. bar = 50 μm.