External factors
| External factors: |
Icariin |
| Category: |
Chemical compounds |
| Tissue type: |
Coronary artery |
| 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. |
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Regulatory relationship
| 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 |
| Official symbol(s): |
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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. |
Aging network
Annotation:
The green line represents Upregulation.
The purple line represents Downregulation.
The orange line represents Activation.
The yellow line represents Inhibition.
The gray line represents Unclear.
Related pathway view