| External factors: | Icariin |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay//Western blot |
| Description: | When HUVECs under 400 μM homocysteine stimulation were treated by ICA (0.1 5 μM), the percentage of SA-β-gal-positive cells were reduced significantly in a dose-dependent manner. |
| Target gene: | AKT//ERK//ENOS |
| R-EF-Target gene: | --//--//-- |
| Official symbol(s): | AKT//ERK//ENOS |
| Target gene experiment: | Western blot |
| Target gene description: | As shown ICA induced rapid AKT phosporylation after 30-min incubation in HUVECs, maximum effects were achieved at ~60min. ERK1/2 phosphorylation was stimulated 10min later, the maximum effects were achieved at 30 60min. Both in HUVECs and in homocysteine-stimulated HUVECs, ICA increased the protein expression of phosphorylated eNOS. |
| Regulatory pathway: | PI3K-Akt-eNOS |
| R-EF-Pathway: | -- |
| Official symbol(s): | PIK3CB-AKT1-NOS3 |
| Pathway experiment: | Measurement of nitrite |
| Pathway description: | The presence of PI3K inhibitor wortmannin abolished most effects of ICA on NO production, while the MEK inhibitor PD98059 did not show this ability . These results suggested that effects of ICA on NO production mainly involved PI3K/AKT-eNOS signaling pathways. |
Annotation: