| External factors: | Metformin |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay//Van Geison staining//Histochemical staining//Flow cytometry//Immunofluorescence |
| Description: | SA-β-gal activity assay:SA-β-gal staining in HAEC, early versus late passage controls, as well as in cells continuously grown in the presence of metformin from p5 to p16，chronic administration of metformin delays endothelial cell senescence. SA-β-gal activity assay:In addition, a significant reduction in the SA-β-gal staining of aorta was observed in metformin-administered mice in comparison to untreated ApoE?/?mice. Van Geison staining//Masson:These changes were further confirmed with Van Geison staining indicating increased presence of collagen tissue and Masson's trichrome staining indicating accumulation of fibrous connective tissue with ruptured medial layer in ApoE?/?mice. |
| Target gene: | AMPKα//HTERT//SIRT1//DOT-1L |
| R-EF-Target gene: | Activation//Upregulation//Upregulation//Upregulation |
| Official symbol(s): | PRKAA1//HTERT//SIRT1//CASP3 |
| Target gene experiment: | Western blot |
| Target gene description: | Western blot：Metformin treatment resulted in a significant activation of AMPKα in early and late passage endothelial cells,albeit, the responsiveness was marginally more in early passage in comparison to late passage cells.Metformin and AICAR significantly increased hTERT levels by 8h. To explore if AMPKα-mediated hTERT expression involves SIRT1 activation, HAEC were treated either with metformin or AICAR and found that these AMPK activators increased SIRT1 levels.To test this, cells were treated either with AICAR or metformin. AMPK activators dose- and time-dependently enhanced DOT-1 L and H3K79 trimethylation (me3) in HAEC . |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: