| External factors: | Resveratrol |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay//Immunohistochemistry//Immunofluorescence |
| Description: | On the other hand, in comparison with the ethanol treatment, the resveratrol treatment obviously increased the level of SIRT1 (increased by 62%, P < 0.05) and the number of Ki67 positive β-cells in islets from the Eth+Res group. Meanwhile, resveratrol decreased the levels of p-p38MAPK and p16 in β-cells and the percentage of SA-β-gal positive area in islets. |
| Target gene: | SIRT1 |
| R-EF-Target gene: | Upregulation |
| Official symbol(s): | SIRT1 |
| Target gene experiment: | Western blot//SA-β-gal activity assay |
| Target gene description: | Moreover, compared with the ethanol+resveratrol group, Ex527 completely abolished the anti-senescence effects of resveratrol by increasing the percentage of SA-β-gal-positive cells (P < 0.001) and activating the p38MAPK/p16 pathway (P < 0.01, P < 0.01) in the Ex527+Res+ethanol group, which further suggested that SIRT1 activation is indeed necessary for the anti-senescence effect of resveratrol. |
| Regulatory pathway: | p38MAPK-p16 |
| R-EF-Pathway: | Downregulation |
| Pathway experiment: | Western blot//SA-β-gal activity assay |
| Pathway description: | As shown in Figure 4, supplementation with SB203580 protected INS-1 cells from ethanol-induced senescence by significantly reducing the percentage of SA-β-gal-positive cells (17.4% vs. 28.2%, P < 0.01) and elevating the expression of the proliferation markers PCNA and Ki67 (P < 0.05). Moreover, several studies have established a critical role for the polycomb group protein Bmi1 in the p38-MAPK/p16 pathway, in which Bmi1 is downregulated by p38MAPK which further activates p16 to induce β-cell senescence. In comparison with ethanol-treated cells, SB203580-treated cells had significantly decreased ethanol-stimulated expression of p16 (decreased by 25%, P < 0.05) but recovered Bmi1 and cyclin D2 levels (increased by 40%, P < 0.05; 125%, P < 0.05, respectively), which indicated that activation of p38MAPK/p16 pathway largely contributed to the ethanol-induced β-cell senescence. |
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