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

As measured by thin-layer chromatography, Galangin inhibits the catabolic breakdown of DMBA in a dose-dependent manner. Galangin also inhibits the formation of DMBA-DNA adducts, and prevents DMBA-induced inhibition of cell growth. Galangin causes a potent, dose-dependent inhibition of CYP1A1 activity, as measured by ethoxyresorufin-O-deethylase activity, in intact cells and in microsomes isolated from DMBA-treated cells. Analysis of the inhibition kinetics by double-reciprocal plot demonstrates that galangin inhibits CYP1A1 activity in a noncompetitive manner. Galangin causes an increase in the level of CYP1A1 mRNA, indicating that it may be an agonist of the aryl hydrocarbon receptor, but it inhibits the induction of CYP1A1 mRNA by DMBA or by 2,3,5,7-tetrachlorodibenzo-p-dioxin (TCDD). Galangin also inhibits the DMBA- or TCDD-induced transcription of a reporter vector containing the CYP1A1 promoter[1]. Galangin treatment inhibits cell proliferation and induced autophagy (130 μM) and apoptosis (370 μM). In particular, galangin treatment in HepG2 cells causes (1) an accumulation of autophagosomes, (2) elevated levels of microtubule-associated protein light chain 3, and (3) an increased percentage of cells with vacuoles. p53 expression is also increased. The galangin-induced autophagy is attenuated by the inhibition of p53 in HepG2 cells, and overexpression of p53 in Hep3B cells restored the galangin-induced higher percentage of cells with vacuoles to normal level[2].

Cells (5.0×103) are seeded and treated with different concentrations of galangin for different periods of time in 96-well plates. The number of viable cells in each well is determined by adding 10 μL of 5 mg/mL MTT solution. Following the 4 hour incubation at 37°C, the cells are dissolved in a 100 μL solution containing 20% SDS and 50% dimethy formamide. The optical densities are quantified at a test wavelength of 570 nm with a reference wavelength of 630 nm using a Varioskan Flash Reader spectrophotometer.

548-83-4

C15H10O5

270.24

Norizalpinin;高良姜素;3,5,7-Trihydroxyflavone;Galangin

[1]Gargouri W, Osés S M. Evaluation of bioactive compounds and biological activities of Tunisian propolis. LWT. 2019 Aug 111:328-336[2]Osés S M, Marcos P, Azofra P, et al. Phenolic Profile, Antioxidant Capacities and Enzymatic Inhibitory Activities of Propolis from Different Geographical Areas: Needs for Analytical Harmonization[J]. Antioxidants. 2020, 9(1): 75.[3]Ciolino HP, et al. The flavonoid galangin is an inhibitor of CYP1A1 activity and an agonist/antagonist of the aryl hydrocarbon receptor. Br J Cancer. 1999 Mar;79(9-10):1340-6.[4]Wen M, et al. Galangin induces autophagy through upregulation of p53 in HepG2 cells. Pharmacology. 2012;89(5-6):247-55.

[1]Lim J, Ferruzzi M G, Hamaker B R. Dietary starch is weight reducing when distally digested in the small intestine. Carbohydrate Polymers. 2021: 118599.[2]Lim J, Ferruzzi M G, Hamaker B R. Structural requirements of flavonoids for the selective inhibition of α-amylase versus α-glucosidase. Food Chemistry. 2022, 370: 130981.[3]Osés S M, Marcos P, Azofra P, et al. Phenolic Profile, Antioxidant Capacities and Enzymatic Inhibitory Activities of Propolis from Different Geographical Areas: Needs for Analytical Harmonization. Antioxidants. 2020, 9(1): 75[4]Gargouri W, Osés S M, Evaluation of bioactive compounds and biological activities of Tunisian propolis. LWT. 2019 Aug 111:328-336

Chloroform, Dichloromethane, Ethyl Acetate, Acetone:Soluble
DMSO:27 mg/mL(100 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years