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Glabridin

$93

  • Brand : BIOFRON

  • Catalogue Number : BF-G2011

  • Specification : 98%

  • CAS number : 59870-68-7

  • Formula : C20H20O4

  • Molecular Weight : 324.37

  • PUBCHEM ID : 124052

  • Volume : 20mg

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Catalogue Number

BF-G2011

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

324.37

Appearance

White needle crystal

Botanical Source

Glycyrrhiza uralensis

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1(C=CC2=C(O1)C=CC3=C2OCC(C3)C4=C(C=C(C=C4)O)O)C

Synonyms

1,3-Benzenediol,4-(3,4-dihydro-8,8-dimethyl-2H,8H-benzo(1,2-b:3,4-b')dipyran-3-yl)-,(R)/4-(3,4-Dihydro-8,8-dimethyl-2H,8H-benzo(1,2-b:3,4-b')dipyran-3-yl)-1,3-benzenediol/Glabridin/Bio-0904/4-[(3R)-8,8-dimethyl-3,4-dihydro-2H-pyrano[2,3-f]chromen-3-yl]benzene-1,3-diol/4-[(3R)-8,8-Dimethyl-3,4-dihydro-2H,8H-pyrano[2,3-f]chromen-3-yl]benzene-1,3-diol/4-[(3R)-8,8-Dimethyl-3,4-dihydro-2H,8H-pyrano[2,3-f]chromen-3-yl]-1,3-benzenediol/1,3-Benzenediol, 4-[(3R)-3,4-dihydro-8,8-dimethyl-2H,8H-benzo[1,2-b:3,4-b']dipyran-3-yl]-

IUPAC Name

4-[(3R)-8,8-dimethyl-3,4-dihydro-2H-pyrano[2,3-f]chromen-3-yl]benzene-1,3-diol

Density

1.3±0.1 g/cm3

Solubility

Methanol; Ethyl Acetate

Flash Point

267.4±30.1 °C

Boiling Point

518.6±50.0 °C at 760 mmHg

Melting Point

154-155ºC

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2932990000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:59870-68-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

30771297

Abstract

Prevention of muscle wasting is known to contribute to improving the quality of life and extending a healthy life. Recently, we have reported that licorice flavonoid oil containing glabridin, which is a prenylated isoflavone, enhances muscle mass in mice. In this study, we investigated the prevention effect of glabridin on dexamethasone-induced muscle atrophy and clarified its mechanism in cultured myotubes and in muscle of mice. Treatment with glabridin to C2C12 myotubes inhibited dexamethasone-induced protein degradation through dexamethasone-induced expression of ubiquitin ligases, MuRF1 and Cbl-b, but not atrogin-1. Mechanistically, glabridin inhibited nuclear translocation of the glucocorticoid receptor. Glabridin directly bound to the glucocorticoid receptor, resulting in the inhibition of binding between dexamethasone and the receptor protein. Glabridin also inhibited dexamethasone-induced phosphorylation of p38 and FoxO3a, as the upstream for the induction of ubiquitin ligases in C2C12 myotubes. Moreover, the glabridin-induced inhibition of protein degradation was eliminated by knockdown of the glucocorticoid receptor, but not by p38 knockdown. These data indicated that the inhibitory mechanism of glabridin against dexamethasone-induced muscle atrophy was mainly mediated by the inhibition of binding between dexamethasone and the glucocorticoid receptor in myotubes. Oral administration of glabridin prevented dexamethasone-induced protein degradation in the tibialis anterior muscle of mice. It was confirmed that glabridin inhibited dexamethasone-induced nuclear translocation of the glucocorticoid receptor and phosphorylation of FoxO3a in the muscle of mice. These findings suggest that glabridin is an effective food ingredient for the prevention of glucocorticoid-induced skeletal muscle atrophy.

Copyright © 2019 Elsevier Inc. All rights reserved.

KEYWORDS

Glabridin; Glucocorticoid receptor; Muscle atrophy

Title

Glabridin inhibits dexamethasone-induced muscle atrophy.

Author

Yoshioka Y1, Kubota Y2, Samukawa Y2, Yamashita Y2, Ashida H3.

Publish date

2019 Mar 30

PMID

30051472

Abstract

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has various toxicological effects in adipose tissue. Evidence is accumulating that glabridin, a flavonoid extracted from licorice, has beneficial effects on the regulation of glucose homeostasis. In this study, we investigated whether glabridin suppresses TCDD-induced loss of adipogenic action using 3T3-L1 adipocytes as a cell culture model of wasting syndrome. Glabridin effectively suppressed TCDD-induced loss of lipid accumulation in this model. Pretreating cells with glabridin increased the gene expression of not only the adipogenesis-associated key transcription factors peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer binding protein alpha, but also lipoprotein lipase in the presence of TCDD. TCDD decreased insulin-stimulated glucose uptake, which was effectively restored by pretreatment with glabridin. Glabridin also inhibited the TCDD-driven decreased production of insulin receptor substrate 1 and glucose transporter 4. TCDD increased the production of mitochondrial superoxides, prostaglandin E2 , phospholipase A2 , cyclooxygenase-1 and intracellular calcium concentrations, while reducing the production of PPARγ coactivator 1 alpha and glycolysis. However, glabridin treatment reduced these TCDD-induced effects. We conclude that glabridin suppresses the TCDD-induced loss of lipid accumulation in 3T3-L1 adipocytes by regulating the levels of PPARγ, CCAAT/enhancer binding protein alpha, lipoprotein lipase, glucose uptake, prostaglandin E2 and energy metabolism. These results also provide in vitro evidence of the effects of glabridin on adipocyte metabolism, which suggests a protective effect against dioxin exposure in the development of insulin resistance and diabetes.

© 2018 John Wiley & Sons, Ltd.

KEYWORDS

2,3,7,8-tetrachlorodibenzo-p-dioxin; 3T3-L1 adipocyte; differentiation; glabridin; prostaglandin E2

Title

Glabridin attenuates antiadipogenic activity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in murine 3T3-L1 adipocytes.

Author

Choi EM1, Suh KS1, Jung WW2, Park SY3,4, Chin SO1,4, Rhee SY1,4, Kim Pak Y5, Chon S1,4.

Publish date

2018 Nov

PMID

29663662

Abstract

Glabridin, a flavonoid extracted from licorice (Glycyrrhiza glabra), possesses various biological properties, including anticancer activities. However, the effect of glabridin on oral cancer cell apoptosis and the underlying molecular mechanisms has not been elucidated. In this study, we demonstrated that glabridin treatment significantly inhibits cell proliferation in human oral cancer SCC-9 and SAS cell lines. Flow cytometric assays demonstrated that glabridin induced several features of apoptosis, such as sub-G1 phase cell increase and phosphatidylserine externalization. Furthermore, glabridin induced apoptosis dose-dependently in SCC-9 cells through caspase-3, -8, and -9 activation and poly (ADP-ribose) polymerase cleavage. Moreover, glabridin increased the phosphorylation of the extracellular signal-regulated kinase, p38, and c-Jun N-terminal kinase (JNK) pathways in a dose-dependent manner. Moreover, the inhibition of the JNK1/2 inhibitor significantly reversed the glabridin-induced activation of the caspase pathway. In conclusion, our findings suggest that glabridin induces oral cancer cell apoptosis through the JNK1/2 pathway and is a potential therapeutic agent for oral cancer.

© 2018 Wiley Periodicals, Inc.

KEYWORDS

JNK1/2 pathway; apoptosis; caspase; glabridin; oral cancer

Title

Glabridin induces apoptosis and cell cycle arrest in oral cancer cells through the JNK1/2 signaling pathway.

Author

Chen CT1,2,3, Chen YT1,2,3, Hsieh YH4, Weng CJ5, Yeh JC1,2,3, Yang SF6,7, Lin CW2,3, Yang JS6,7.

Publish date

2018 Jun


Description :

Glabridin is a natural isoflavan from Glycyrrhiza glabra, binds to and activates PPARγ, with an EC50 of 6115 nM. Glabridin exhibits antioxidant, anti-bacterial, anti-nephritic, anti-diabetic, anti-fungal, antitumor, anti-inflammatory, antiosteoporotic, cardiovascular protective, neuroprotective and radical scavenging activities[1][2].