| External factors: | 2-O-α-glucopyranosyl-L-ascorbic acid |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay |
| Description: | We investigated the effects of AA-2G on NHDF cell growth and against H2O2-induced cell damage. Pretreatment of NHDF cells with AA-2G for 72 h significantly promoted the cell growth in a dosedependent manner.Pretreatment with AA-2G for 72 h slightly but significantly decreased SA-β-gal activity in H2O2-unexposed NHDF cells. |
| Target gene: | SIRT1//P53//P21 |
| R-EF-Target gene: | --//Downregulation//Downregulation |
| Official symbol(s): | SIRT1//P53//P21 |
| Target gene experiment: | Western blot//ELISA |
| Target gene description: | Neither ascorbic acid nor AA-2G alone affected SIRT1 expression when they were added to cell cultures. In contrast, when NHDF cells were exposed to H2O2, SIRT1 expression levels were significantly decreased compared to unexposed cells. Pretreatment of NHDF cells with 200 μM AA-2G for 72 h significantly inhibited the H2O2-induced decrease in SIRT1 expression. However, pretreatment with 200 μM ascorbic acid did not inhibit the H2O2-induced decrease of the SIRT1 expression. These results suggest that AA-2G prevents oxidative stress-induced cellular senescence in terms of both SA-β-gal activity and SIRT1 expression.To further clarify the anti-aging effect of AA-2G, we examined the expression levels of p53 and p21 in H2O2-exposed NHDF cells.Constitutive expression of p53 was observed in AA-2G untreated cells. Its expression level was elevated by H2O2 exposure, and reached maximum levels at 4 h postexposure. Pretreatment with 200 μM AA2G for 72 h resulted in a decrease in both constitutive and H2O2-induced expression of p53. Exposure of NHDF cells to H2O2 also resulted in increased expression of p21 in AA-2G untreated cells compared with that in H2O2-unexposed cells. The expression reached maximum levels at 4 h postexposure. These results suggest that cell cycle arrest at G1 phase is induced by H2O2-exposure. Pretreatment with 200 μM AA-2G inhibited the expression of p21 in the H2O2-exposed cells. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: