Liquiritigenin, a flavonoid aglycone from licorice, has a choleretic effect and the ability to induce hepatic transporters and phase-II enzymes | Health & Environmental Research Online (HERO)

HERO ID

880765

Reference Type

Journal Article

Title

Liquiritigenin, a flavonoid aglycone from licorice, has a choleretic effect and the ability to induce hepatic transporters and phase-II enzymes

Author(s)

Kim, YW; Kang, HE; Lee, MG; Hwang, SJ; Kim, SC; Lee, CH; Kim, SG

Year

2009

Is Peer Reviewed?

Yes

Journal

American Journal of Physiology: Gastrointestinal and Liver Physiology
ISSN: 0193-1857
EISSN: 1522-1547

Volume

296

Issue

2

Page Numbers

G372-G381

Language

English

PMID

19074639

DOI

10.1152/ajpgi.90524.2008

Web of Science Id

WOS:000262782200027

URL

https://www.physiology.org/doi/10.1152/ajpgi.90524.2008
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Abstract

Liquiritigenin (LQ), an active component of licorice, has an inhibitory effect on LPS-induced inhibitory nitric oxide synthase expression. This study investigated the effects of LQ on choleresis, the expression of hepatic transporters and phase-II enzymes, and fulminant hepatitis. The choleretic effect and the pharmacokinetics of LQ and its glucuronides were monitored in rats. After intravenous administration of LQ, the total area under the plasma concentration-time curve of glucuronyl metabolites was greater than that of LQ in plasma, which accompanied elevations in bile flow rate and biliary excretion of bile acid, glutathione, and bilirubin. The expressions of hepatocellular transporters and phase-II enzymes were assessed by immunoblots, real-time PCR, and immunohistochemistry. In the livers of rats treated with LQ, the protein and mRNA levels of multidrug resistance protein 2 and bile salt export pump were increased in the liver, which was verified by their increased localizations in canalicular membrane. In addition, LQ treatment enhanced the expression levels of major hepatic phase-II enzymes. Consistent with these results, LQ treatments attenuated galactosamine/LPS-induced hepatitis in rats, as supported by decreases in the plasma alanine aminotransferase, liver necrosis, and plasma TNF-alpha. These results demonstrate that LQ has a choleretic effect and the ability to induce transporters and phase-II enzymes in the liver, which may be associated with a hepatoprotective effect against galactosamine/LPS. Our findings may provide insight into understanding the action of LQ and its therapeutic use for liver disease.

Keywords

choleresis; hepatocellular transporter; glucuronidation