Description |
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].
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In Vitro |
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.
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In Vivo |
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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Density | 1.3±0.1 g/cm3 |
Boiling Point | 588.6±50.0 °C at 760 mmHg |
Flash Point | 309.8±30.1 °C |
Exact Mass | 354.146729 |
PSA | 79.15000 |
LogP | 6.48 |
Vapour Pressure | 0.0±1.7 mmHg at 25°C |