| External factors: | Salicin |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Vascular disease |
| Experiment: | SA-β-gal activity assay//Flow cytometry |
| Description: | When endothelial cells were exposed to 10 ng/mL TNF-a, those not treated by salicin displayed significantly greater cellular senescence after 48 h, as compared to cells that were not exposed to TNF-a. In contrast, salicin prevented senescence in a dose-dependent manner; endothelial cells treated with 50 and 100 mM of salicin showed proportionately less cellular senescence, with the 100 mM assay relative SA-β-Gal level of the 100 mM assay approaching that of the assay not treated with TNF-a.Cell cycle analysis indicated that whereas TNF-a-affected cells showed a higher level of cell cycle dysfunction compared to cells that were not exposed to TNF-a, salicin demonstrated a protective effect against cell cycle disruption at G0/G1. |
| Target gene: | NRF2 |
| R-EF-Target gene: | -- |
| Official symbol(s): | NRF2 |
| Target gene experiment: | Western blot |
| Target gene description: | While nuclear levels of NRF2 were reduced in the group exposed to TNF-a, replicating previous research that TNF-a hinders nuclear translocation of NRF2. Importantly, we found that salicin promoted nuclear translocation of NRF2. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: