| External factors: | Oxytocin |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay//Western blot//Knockdown |
| Description: | OXTR knockdown or treatment with a MAPK kinase (MEK) inhibitor completely abolished the ability of OT to prevent the SASP-induced cellular senescence, as indicated by increased SA-β-Gal positive rate, upregulated levels of p21 and p16, and diminished cell proliferation. |
| Regulatory pathway: | ERK-Nrf2 |
| R-EF-Pathway: | Activation |
| Official symbol(s): | ERK-NFE2L2 |
| Pathway experiment: | SA-β-gal activity assay//Western blot//Knockdown |
| Pathway description: | OT enhanced nuclear accumulation of Nrf2 in a dose-dependent manner . This was reversed by OXTR silencing or treatment with MEK inhibitor .Knockdown of Nrf2 completely abrogated the beneficial effects of OT on SASP-induced senescence . |
Annotation: