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Galangin

$113

  • Brand : BIOFRON

  • Catalogue Number : BF-G2012

  • Specification : 98%

  • CAS number : 548-83-4

  • Formula : C15H10O5

  • Molecular Weight : 270.24

  • PUBCHEM ID : 5281616

  • Volume : 20mg

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Catalogue Number

BF-G2012

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

270.24

Appearance

Light yellow crystalline powder

Botanical Source

Eriobotrya japonica,Glycyrrhiza uralensis,Pinus tabuliformis,Populus × canadensis,Populus davidiana

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC=C(C=C1)C2=C(C(=O)C3=C(C=C(C=C3O2)O)O)O

Synonyms

3,5,7-trihydroxyflavone/Galangin/teptochrysin/Galengin/3,5,7-trihydroxy-2-phenyl-chromen-4-one/3,5,7-trihydroxy-flavon/3,5,7-Trihydroxy-2-phenyl-4H-chromen-4-one/3,5,7-Trihydroxy-Flavone/galangine/5,7-dihydroxyflavonol/4H-1-Benzopyran-4-one, 3,5,7-trihydroxy-2-phenyl-/NORIZALPININ/3,5,7-trihydroxyfalvone/3,5,7-Trihydroxy-2-phenyl-4H-1-benzopyran-4-one

IUPAC Name

3,5,7-trihydroxy-2-phenylchromen-4-one

Density

1.6±0.1 g/cm3

Solubility

Methanol

Flash Point

202.0±23.6 °C

Boiling Point

518.6±50.0 °C at 760 mmHg

Melting Point

214-215 °C(lit.)

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#:548-83-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

32235536

Abstract

Among women worldwide, ovarian cancer is one of the most dangerous cancers. Patients undergoing platinum-based chemotherapy might get adverse side effects and develop resistance to drugs. In recent years, natural compounds have aroused growing attention in cancer treatment. Galangin inhibited the growth of two cell lines, A2780/CP70 and OVCAR-3, more strongly than the growth of a normal ovarian cell line, IOSE 364. The IC50 values of galangin on proliferation of A2780/CP70, OVCAR-3 and IOSE 364 cells were 42.3, 34.5, and 131.3 μM, respectively. Flow cytometry analysis indicated that galangin preferentially induced apoptosis in both ovarian cancer cells with respect to normal ovarian cells. Galangin treatment increased the level of cleaved caspase-3 and -7 via the p53-dependent intrinsic apoptotic pathway by up-regulating Bax protein and via the p53-dependent extrinsic apoptotic pathway by up-regulating DR5 protein. By down-regulating the level of p53 with 20 μM pifithrin-α (PFT-α), the apoptotic rates of OVCAR-3 cells induced by galangin treatment (40 μM) were significantly decreased from 18.2% to 10.2%, indicating that p53 is a key regulatory protein in galangin-induced apoptosis in ovarian cancer cells. Although galangin up-regulated the expression of p21, it had little effect on the cell cycle of the two ovarian cancer cell lines. Furthermore, the levels of phosphorylated Akt and phosphorylated p70S6K were decreased through galangin treatment, suggesting that the Akt/p70S6K pathways might be involved in the apoptosis. Our results suggested that galangin is selective against cancer cells and can be used for the treatment of platinum-resistant ovarian cancers in humans.

KEYWORDS

antioxidants; apoptosis; flavonoid; galangin; ovarian cancer; western blot

Title

Galangin, a Flavonoid from Lesser Galangal, Induced Apoptosis via p53-Dependent Pathway in Ovarian Cancer Cells.

Author

Huang H1,2, Chen AY3, Ye X4, Guan R5, Rankin GO6, Chen YC2.

Publish date

2020 Mar 30

PMID

32013062

Abstract

Galangin is a natural flavonoid that has been reported to provide substantial health benefits. Nevertheless, little is known about the potential effects of galangin against inflammatory bowel diseases. Here, an in vivo study was performed to investigate the preventive effects of galangin against dextran sulphate sodium (DSS)-induced acute murine colitis, which mimics the symptoms of human ulcerative colitis (UC). Pre-treatment with galangin (15 mg/kg, p.o.) resulted in a significant decreased in the macroscopic signs of DSS-induced colitic symptoms, including a decreased disease activity index, prevention of the colon length shortening, and alleviation of the pathological changes occurring in the colon. Colonic pro-inflammatory mediators, including tumor necrosis factor-alpha, interleukin (IL)-1 beta, and IL-6, as well as myeloperoxidase activities were decreased following galangin pre-treatment when compared with the DSS control group. Moreover, galangin pre-treatment significantly increased the expressions of autophagy-related proteins and promoted the formation of autophagosome in the colon. Galangin pre-treatment increased the diversity of the gut microbiota, and this was accompanied by increased levels of short-chain fatty acids. These observed changes could involve the modulating effects conferred by galangin in relation to some specific bacteria populations, including the recovery of Lactobacillus spp., and increased Butyricimonas spp. Overall, these results support the use of galangin in the prevention of UC.

Title

Galangin Protects against Symptoms of Dextran Sodium Sulfate-induced Acute Colitis by Activating Autophagy and Modulating the Gut Microbiota.

Author

Xuan H1,2, Ou A3, Hao S4, Shi J5, Jin X2.

Publish date

2020 Jan 29

PMID

31528214

Abstract

Galangin (3,5,7‑trihydroxyflavone), a natural flavonoid present in plants, has been reported to possess anticancer properties in various types of cancers comprising glioma. The underlying mechanism, however, has not been fully elucidated. CD44, a hall marker in glioma, has been reported to be associated with epithelial-mesenchymal transition (EMT) and angiogenesis, which play important roles in glioma progression. In this study, we aimed to investigate whether galangin can inhibit EMT, angiogenesis and CD44 expression in glioma. We observed that galangin inhibited the proliferation, migration, invasion and angiogenesis of glioma cells in a dose-dependent manner, suppressed the expression of CD44 and inhibited angiogenesis of glioma cells through downregulating vascular endothelial growth factor (VEGF) in HUVECs. In addition, the overexpression of CD44 in U87 and U251 cells partly abolished the effects of galangin on glioma cells. Moreover, galangin suppressed tumor growth in an intracranial glioma mouse model. These results indicate that galangin is a potential novel drug for glioblastoma treatment due to its ability to suppress of CD44, EMT and angiogenesis.

KEYWORDS

CD44; EMT; galangin; glioblastoma; suppression

Title

Galangin inhibits epithelial-mesenchymal transition and angiogenesis by downregulating CD44 in glioma.

Author

Chen D1, Li D2, Xu XB1, Qiu S1, Luo S1, Qiu E1, Rong Z1, Zhang J1,2, Zheng D1,2.

Publish date

2019 Jul 25


Description :

Galangin is an agonist/antagonist of the arylhydrocarbon receptor, and also shows inhibition of CYP1A1 activity.