Dehydroglyasperin C |
| Catalog No.GC66362 |
La déhydroglycasperine C, une isoflavone, est un puissant NAD(P)H:oxydoquinone réductase (NQO1) et un inducteur enzymatique de phase 2. La déshydroglycasperine C a des activités antioxydantes, neuroprotectrices, chimiopréventives du cancer et anti-inflammatoires.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 199331-35-6
Sample solution is provided at 25 µL, 10mM.
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Dehydroglyasperin C, a isoflavone, is a potent NAD(P)H:oxidoquinone reductase (NQO1) and phase 2 enzyme inducer. Dehydroglyasperin C has antioxidant, neuroprotective, cancer chemopreventive, and anti-inflammatory activities[1][2][3].
Dehydroglyasperin C (0.1-1 μM; 24 h) blocks the PDGF-induced progression through the G0/G1 to S phase of the cell cycle, and down-regulates the expression of CDK; 2, cyclin E, CDK4 and cyclin D1. Dehydroglyasperin C significantly attenuates PDGF-stimulated phosphorylation of PDGF receptor-β, phospholipase C-γ1, AKT and extracellular-regulated kinase 1/2, and DGC inhibits cell migration and the dissociation of actin filaments by PDGF[1].
Dehydroglyasperin C (0.1-1 μM; 24 h) treatment significantly decreases PDGF-induced cell number and DNA synthesis in a dose-dependent manner without any cytotoxicity in human aortic smooth muscle cells (HASMC)[1].
Cell Cycle Analysis[1]
| Cell Line: | Human aortic smooth muscle cells (HASMC) |
| Concentration: | 0.1 μM, 0.5 μM, 1 μM |
| Incubation Time: | 24 hours |
| Result: | Blocked the PDGF-induced progression through the G0/G1 to S phase of the cell cycle. |
Western Blot Analysis[1]
| Cell Line: | Human aortic smooth muscle cells (HASMC) |
| Concentration: | 0.1 μM, 0.5 μM, 1 μM |
| Incubation Time: | 24 hours |
| Result: | Down-regulated the expression of CDK; 2, cyclin E, CDK4 and cyclin D1. |
In ICR mice, Dehydroglyasperin C (5 mg/kg; once) combined with CCl4 shows reduced lipid droplet formation in liver tissue, as assessed by histological examination. Further, DGC demonstrated a slight protective effect against centrilobular injury caused by CCl4 injection, perhaps through suppression of CYP2E1 expression[4].
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