| External factors: | Vildagliptin |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Osteoarthritis |
| Experiment: | SA-β-gal activity assay |
| Description: | When vildagliptin was included in the experiment, it showed a strong suppression of SAβ-Gal activity, with an SA-β-Gal reading of about 17,000 Fu/mg. |
| Target gene: | P53//SIRT1//AMPK |
| R-EF-Target gene: | --//--//-- |
| Official symbol(s): | P53//SIRT1//PRKAA2 |
| Target gene experiment: | Western blot//IP |
| Target gene description: | Compared to the nontreated chondrocytes, TNF-α induced an average of roughly 3.2-fold higher K382 acetylation of p53. The same TNF-α treatment only induced roughly 2.4- and 1.6-fold higher p53 K382 acetylation in the presence of 5 and 10 μM vildagliptin, respectively.Compared to nontreated chondrocytes, TNF-α caused a 75% reduction in SIRT1 protein expression. However, TNF-α only caused a 65% and 40% reduction in SIRT1 when 5 and 10 μM concentrations of vildagliptin were present in the media, respectively. Compared to nontreated cells, the total AMPK level remained the same, but TNF-α caused a roughly 75% reduction in p-AMPK. However, the same TNF-α treatment only caused roughly 50% and 25% reductions in p-AMPK in the presence of two doses of vildagliptin, respectively. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: