External factors: | 2,3,5,40-tetrahydroxystilbene-2-O-b-D-glucoside |
Aging type: | Prevent |
Aging characteristic: |
Category: | Chemical compounds |
Phenotype: | Aging |
Experiment: | SA-β-gal activity assay//Immunofluorescence |
Description: | After stimulation with H2O2 for 1 h and washing out, incubation with THSG for 4 days effectively counteracted H2O2-induced premature senescence in a dose-dependent manner.THSG inhibited vascular senescence in aortic arches .frozen section stain analysis of immunofluorescence of anti-p-gH2AX, a marker of senescence, showed that THSG treatment inhibited phosphorylation of gH2AX in SHRs, although smooth muscle a-actinin (SMA) did not exhibit any remarkable changes . |
Target gene: | ENOS//P53 |
R-EF-Target gene: | Upregulation//Downregulation |
Official symbol(s): | ENOS//P53 |
Target gene experiment: | Western blot//qRT-PCR//Luciferase reporter assay |
Target gene description: | Using an eNOS promoter reporter luciferase, we found that THSG produced a 3-fold increase in eNOS reporter gene luciferase activity of the peaks.Results of our animal experiments also demonstrated that administration of THSG restored eNOS expression in aortas of SHRs.In aortas of rats, Western blot analysis demonstrated that THSG treatment significantly restricted expression and K373 acetylation of p53 compared with control SHRs. |
Regulatory pathway: | SIRT1 |
R-EF-Pathway: | Upregulation |
Official symbol(s): | SIRT1 |
Pathway experiment: | Western blot |
Pathway description: | THSG activated faintly SirT1 activity in vitro compared with resveratrol.quantitative RT-PCR revealed a pattern of decreasing expression of Sirt1, Sirt3, and Sirt6 in aortas of control SHRs compared with WKY rats, however, administration of THSG restored and elevated expression of these proteins. |
Annotation: