| External factors: | Salidroside |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experimental category: | L |
| Tissue type: | -- |
| Cell name: | Aortic Endothelial cell,Smooth muscle cell,HUVEC |
| PMID: | 29289557 |
| Experiment: | SA-β-gal activity assay//Immunostaining |
| Description: | When comparing with control group, the cells of aortic endothelium and smooth muscle in mice with chronic HMD treatment showed accelerated up-regulation of p16 INK4A and p21 CIP1. However, SAL treatment abolished these changes in blood vessels. H2O2 induced the upregulation of SA-β-Gal activity, which indicated that the HUVECs were indeed undergoing senescence.SAL treatment at the concentration of 10 uM inhibited the activity of SA-β-Gal. |
| Target gene: | SIRT3 |
| R-EF-Target gene: | Upregulation |
| Official symbol(s): | SIRT3 |
| Target gene experiment: | Western blot |
| Target gene description: | B HMD treatment significantly reduced the expression of SIRT3. However, the SAL treatment attenuated the reduced expression of SIRT3. SAL reversed the inhibitory effect of H2O2 on the expression of SIRT3 and endothelial nitric oxide synthase (eNOS). |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: