| External factors: | Montelukast |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Osteoarthritis |
| Experiment: | SA-β-gal activity assay//Immunostaining//Flow cytometry |
| Description: | However,treatment with the specific cysLTR1 antagonist montelukast (10 and 20μM) ameliorated TNF-α-induced elevation of SA-β-Gal activity.Treatment with TNF-α (10 ng/ml) significantly increased γ-H2AX foci formation, which was prevented by montelukast in a dose-dependent manner. However, treatment with montelukast (10 and 20 μM)reduced the proportion of cells in the G0/G1 phase to 55.6% and 52.1%, respectively. |
| Regulatory pathway: | SIRT1-p53 |
| R-EF-Pathway: | -- |
| Official symbol(s): | SIRT1-TP53 |
| Pathway experiment: | IP//Western blot |
| Pathway description: | Immunoprecipitation assay results indicate that TNF-α significantly enhanced p53 K382 acetylation, which was inhibited by montelukast.The results indicate that TNF-α significantly reduced expression of SIRT1, which was prevented by montelukast in a concentration-dependent manner.Silencing of SIRT1 blocked the inhibitory effects of montelukast on p53 K382 acetylation. |
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