Dehydroglyasperin C

Names

[ CAS No. ]:
199331-35-6

[ Name ]:
Dehydroglyasperin C

[Synonym ]:
1,3-Benzenediol, 4-[7-hydroxy-5-methoxy-6-(3-methyl-2-buten-1-yl)-2H-1-benzopyran-3-yl]-
4-((R)-7-Hydroxy-5-methoxy-6-(3-methyl-but-2-enyl)-1-benzopyran-3-yl)-benzene-1,3-diol
4-[7-Hydroxy-5-methoxy-6-(3-methyl-but-2-enyl)-2H-1-benzopyran-3-yl]-benzene-1,3-diol
4-[(R)-7-Hydroxy-5-methoxy-6-(3-methyl-but-2-enyl)-1-benzopyran-3-yl]-benzene-1,3-diol
4-[7-Hydroxy-5-methoxy-6-(3-methyl-2-buten-1-yl)-2H-chromen-3-yl]-1,3-benzenediol

Biological Activity

[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].

[Related Catalog]:

Research Areas >> Cancer

Signaling Pathways >> Others >> Others

Research Areas >> Inflammation/Immunology

Research Areas >> Neurological Disease

[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.

[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].

[References]

[1]. Hyo Jung Kim, et al. Dehydroglyasperin C, a component of liquorice, attenuates proliferation and migration induced by platelet-derived growth factor in human arterial smooth muscle cells. Br J Nutr. 2013 Aug 28;110(3):391-400.

[2]. Ji Hoon Lee, et al. Dehydroglyasperin C suppresses TPA-induced cell transformation through direct inhibition of MKK4 and PI3K. Mol Carcinog. 2016 May;55(5):552-62.

[3]. Ji Yeon Seo, et al. Dehydroglyasperin C isolated from licorice caused Nrf2-mediated induction of detoxifying enzymes. J Agric Food Chem. 2010 Feb 10;58(3):1603-8.

[4]. Seo, J.Y, et al. Protective effects of dehydroglyasperin c against carbon tetrachloride-induced liver damage in mice. Food Sci Biotechnol 23, 547–553 (2014).