| External factors: | Hydrogen sulfide |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay//Flow cytometry//MTT assay |
| Description: | Examination of SA-β-gal activity in HUVECs treated with H2O2 (25 μM) revealed a significant increase in SA-β-galpositive cells, which reached 11.2±1.06%. However, increases in SA-β-gal-positive cells were significantly attenuated in the NaHS (60 μM) group.Our results demonstrated that treatment with 25 μM H2O2 arrested HUVECs in the G0/G1 phase as the proportion of cells in the G0/G1 phase was ~70.2% compared to 54.4% in the control group. NaHS (60 μM) pretreatment eliminate Our study indicated that NaHS (60 μM) improved H2O2-induced decreases in HUVEC proliferation. d the effects of H2O2 and reduced the proportion of cells in the G0/G1 phase to 58.1%. These results indicate that H2S protects against HUVEC senescence. |
| 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 the H2O2 (25 μM) treatment group compared to the control, and NaHS (60 μM) treatment did not rescue SIRT1 expression. In contrast to its effect on protein expression, NaHS enhanced SIRT1 deacetylase activity in vitro, indicating a direct effect on SIRT1-mediated pathways. |
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