| External factors: | Salidroside |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay//Flow cytometry |
| Description: | SAL significantly delayed replicative senescence of 2BS cells by at least 8 PDs (see Table 1). The two concentrations of SAL (5 μM and 10 μM) showed a similar gain in PDs. The growth rate of SAL-treated cells was dramatically increased compared to that of the control cells (Table 1). For the SA-β-gal activity,a biomarker of cellular senescence, only sporadic SA-β-galpositive cells were observed in young control cells. As anticipated, SA-β-gal activity was markedly elevated in 55PD control cells (91 7±7 1%), while cells at 55PD cultured in a 10 μM SAL-supplemented medium from 30PD showed a much lower positive rate (28 3±4 9%).Moreover, SAL treatment for 48 h significantly suppressed the elevated production of intracellular ROS in nearsenescent 2BS cells (50PD). |
| Regulatory pathway: | miR-22-SIRT1 |
| R-EF-Pathway: | -- |
| Official symbol(s): | MIR22-SIRT1 |
| Pathway experiment: | Knockdown//SA-β-gal activity assay//Western blot//qRT-PCR |
| Pathway description: | LentiPre22-infected cells showed a five fold increase of mature miR-22 compared with the young control cells and exhibited an enlarged senescence morphology and SA-β-gal-positive staining , accompanied with an increased protein level of senescenceassociated molecules p53, p21, and p16 . As anticipated, a decreased SIRT1 protein expression was observed in the Lenti-Pre22-infected cells . However, SAL could partly impede the senescence progression induced by lenti-Pre-miR-22. The increment of SA-βgal activity induced by overexpression of miR-22 was prevented in part by SAL. Besides, declined expression of SIRT1 and increased protein levels of p53, p21, and p16 in Lenti-Pre22-infected cells were partly reversed by SAL treatment. These results implied that SAL stimulates the SIRT1 partly through inhibition on miR-22. |
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