External factors
| External factors: |
Rivaroxaban |
| Category: |
Chemical compounds |
| Phenotype: |
Atherosclerosis |
| Experiment: |
SA-β-gal activity assay//Western blot//Flow cytometry |
| Description: |
Coincubation with XaI (rivaroxaban, 50 and 500 nM) significantly decreased SA-β-gal activity. Both 50 and 500 nM rivaroxaban significantly decreased p53 and p16 levels under HG conditions.Additionally,telomere length, an index of replicative senescence, was significantly shortened under HG for 30 days, and it was restored by coincubation with rivaroxaban. |
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Regulatory relationship
| Target gene:
|
P22PHOX//ICAM//VCAM1//PAR1 |
| R-EF-Target gene:
|
Downregulation//Downregulation//Downregulation//Downregulation |
| Official symbol(s): |
P22PHOX//ICAM1//VCAM1//NR1I2 |
| Target gene experiment: |
Western blot |
| Target gene description: |
HG conditions also increased the expression of p22phox, and compared to HG-only conditions, exposure to rivaroxaban significantly restored p22phox expression.ICAM1 and VCAM1, adhesion molecules expressed on vascular endothelial cells, significantly increased under HG, and this increase was significantly reversed by rivaroxaban.PAR1 is involved in the inactivation of eNOS, which is increased under HG conditions and significantly suppressed by rivaroxaban. |
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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.
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