External factors
| External factors: |
Vildagliptin |
| Category: |
Chemical compounds |
| Phenotype: |
Osteoarthritis |
| Cell name: |
Human primary Chondrocyte |
| 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. |
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Regulatory relationship
| 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. |
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Aging network
Annotation:
The green line represents Upregulation.
The purple line represents Downregulation.
The orange line represents Activation.
The yellow line represents Inhibition.
The gray line represents Unclear.
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