Anti-carcinogenic effects of non-polar components containing licochalcone A in roasted licorice root.
- Author:
So Young PARK
1
;
Eun Ji KIM
;
Hyun Ju CHOI
;
Mi Ra SEON
;
Soon Sung LIM
;
Young Hee KANG
;
Myung Sook CHOI
;
Ki Won LEE
;
Jung Han YOON PARK
Author Information
- Publication Type:Original Article
- Keywords: Roasted licorice roots; apoptosis; licochalcone A; cancer
- MeSH: Animals; Anticarcinogenic Agents*; Apoptosis; Blotting, Western; Breast; Carcinogenesis; Colonic Neoplasms; Edema; Epithelial Cells; Ethanol; Fibroblasts; Flow Cytometry; Glycyrrhetinic Acid; Glycyrrhiza*; Glycyrrhizic Acid; Hypertension; Magnetic Resonance Spectroscopy; Melanoma; Metabolism; Methylene Chloride; Mice; Papilloma; Prostatic Neoplasms; Skin; Skin Neoplasms; Spectrum Analysis
- From:Nutrition Research and Practice 2014;8(3):257-266
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/OBJECTIVE: Licorice has been shown to possess cancer chemopreventive effects. However, glycyrrhizin, a major component in licorice, was found to interfere with steroid metabolism and cause edema and hypertension. The roasting process of licorice modifies the chemical composition and converts glycyrrhizin to glycyrrhetinic acid. The purpose of this study was to examine the anti-carcinogenic effects of the ethanol extract of roasted licorice (EERL) and to identify the active compound in EERL. MATERIALS/METHODS: Ethanol and aqueous extracts of roasted and un-roasted licorice were prepared. The active fraction was separated from the methylene chloride (MC)-soluble fraction of EERL and the structure of the purified compound was determined by nuclear magnetic resonance spectroscopy. The anti-carcinogenic effects of licorice extracts and licochalcone A was evaluated using a MTT assay, Western blot, flow cytometry, and two-stage skin carcinogenesis model. RESULTS: EERL was determined to be more potent and efficacious than the ethanol extract of un-roasted licorice in inhibiting the growth of DU145 and MLL prostate cancer cells, as well as HT-29 colon cancer cells. The aqueous extracts of un-roasted and roasted licorice showed minimal effects on cell growth. EERL potently inhibited growth of MCF-7 and MDA-MB-231 breast, B16-F10 melanoma, and A375 and A2058 skin cancer cells, whereas EERL slightly stimulated the growth of normal IEC-6 intestinal epithelial cells and CCD118SK fibroblasts. The MC-soluble fraction was more efficacious than EERL in inhibiting DU145 cell growth. Licochalcone A was isolated from the MC fraction and identified as the active compound of EERL. Both EERL and licochalcone A induced apoptosis of DU145 cells. EERL potently inhibited chemically-induced skin papilloma formation in mice. CONCLUSIONS: Non-polar compounds in EERL exert potent anti-carcinogenic effects, and that roasted rather than un-roasted licorice should be favored as a cancer preventive agent, whether being used as an additive to food or medicine preparations.
