| External factors: | Honokiol |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Disc degenerative disease |
| Experiment: | SA-β-gal activity assay//Western blot |
| Description: | We found that the percentage of SA-β-gal-positive cells was increased in the oxidative stress group when these cells transfected with scramble lentivirus, while HKL treatment could reduce the proportion of senescent NPCs via SIRT3,While HKL treatment could reduce the proportion of senescent NPCs via SIRT3 activation, which was further confirmed by the Western blot analysis of p16INKa. |
| Regulatory pathway: | AMPK-PGC-1α-SIRT3 |
| R-EF-Pathway: | Activation |
| Official symbol(s): | AMPK-PPARGC1A-SIRT3 |
| Pathway experiment: | Western blot |
| Pathway description: | Our results showed that HKL could promote the ratio of p-AMPK to AMPK and the levels of PGC-1α and SIRT3 in a dose-dependent manner in NPCs. Compared with the control group, Compound C reduced the ratio of p-AMPK to AMPK with decreasing levels of PGC-1α and SIRT3, indicating that PGC-1α and SIRT3 were regulated by AMPK.With the administration of HKL, NPCs displayed decreased expression of SIRT3 in the PGC-1α-siRNA group, suggesting that SIRT3 is regulated by PGC-1α in HKL-treated NPCs. |
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