TitleEvidence for Chemopreventive and Resilience Activity of Licorice: and G. Extracts Modulate Estrogen Metabolism in ACI Rats.
Publication TypeJournal Article
Year of Publication2018
AuthorsWang S, Dunlap TL, Huang L, Liu Y, Simmler C, Lantvit DD, Crosby J, Howell CE, Dong H, Chen S-N, Pauli GF, van Breemen RB, Dietz BM, Bolton JL
JournalCancer Prev Res (Phila)
Volume11
Issue12
Pagination819-830
Date Published2018 12
ISSN1940-6215
Abstract

Women are increasingly using botanical dietary supplements (BDS) to reduce menopausal hot flashes. Although licorice ( sp.) is one of the frequently used ingredients in BDS, the exact plant species is often not identified. We previously showed that in breast epithelial cells (MCF-10A), (GG) and (GI), and their compounds differentially modulated P450 1A1 and P450 1B1 gene expression, which are responsible for estrogen detoxification and genotoxicity, respectively. GG and isoliquiritigenin (LigC) increased , whereas GI and its marker compound, licochalcone A (LicA), decreased and The objective of this study was to determine the distribution of the bioactive licorice compounds, the metabolism of LicA, and whether GG, GI, and/or pure LicA modulate NAD(P)H quinone oxidoreductase (NQO1) in an ACI rat model. In addition, the effect of licorice extracts and compounds on biomarkers of estrogen chemoprevention () as well as carcinogenesis () was studied. LicA was extensively glucuronidated and formed GSH adducts; however, free LicA as well as LigC were bioavailable in target tissues after oral intake of licorice extracts. GG, GI, and LicA caused induction of NQO1 activity in the liver. In mammary tissue, GI increased and decreased , whereas GG only increased LigC may have contributed to the upregulation of after GG and GI administration. In contrast, LicA was responsible for GI-mediated downregulation of These studies highlight the polypharmacologic nature of botanicals and the importance of standardization of licorice BDS to specific species and to multiple constituents.

DOI10.1158/1940-6207.CAPR-18-0178
Alternate JournalCancer Prev Res (Phila)
PubMed ID30287522
PubMed Central IDPMC6435032
Grant ListP41 GM068944 / GM / NIGMS NIH HHS / United States
P50 AT000155 / AT / NCCIH NIH HHS / United States
U41 AT008706 / AT / NCCIH NIH HHS / United States