| External factors: | Donepezil |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Alzheimer’s disease |
| Experiment: | MTT assay//Western blot//qRT-PCR//SA-β-gal activity assay//Flow cytometry |
| Description: | The rate of SA-?-gal-positive cells was significantly higher in the HG (30 mmol/L) group compared with the NG (5.6 mmol/L) group, and this increase was suppressed by treatment with donepezil in a concentrationdependent manner from 10 to 50 μM. Our results demonstrated that treatment with 30 mmol/L glucose arrested HUVECs in the G0/G1 phase as the proportion of cells in the G0/G1 phase was~69.9 % compared to 53.3 % in the NG (5.6 mmol/L) group. Donepezil (20 μM) pretreatment eliminated the effects of HG and reduced the proportion of cells in the G0/ G1 phase to 55.3 % . Next, we examined the impact of donepezil on cell viability. Treatment with HG (30 mmol/L) significantly suppressed endothelial cell viability, which was reversed by treatment with donepezil in a concentration dependent manner from 10 to 50 μM.HG treatment drastically increased the expression of PAI-1 and p21, which was markedly suppressed by donepezil treatment . This result was confirmed by Western blot analysis at protein levels. |
| Regulatory pathway: | SIRT1 |
| R-EF-Pathway: | Activation |
| Official symbol(s): | SIRT1 |
| Pathway experiment: | Western blot |
| Pathway description: | Immunoblot analyses indicated that SIRT1 levels were decreased in response to treatment with HG (30 mmol/L), which was partially rescued by treatment with donepezil. SIRT1 deacetylase activity was reduced by treatment with HG. However, donepezil restored the deacetylase activity of SIRT1, indicating a direct effect on SIRT1-mediated pathways. |
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