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

@article{Kim2009LiquiritigeninAF,
  title={Liquiritigenin, a flavonoid aglycone from licorice, has a choleretic effect and the ability to induce hepatic transporters and phase-II enzymes.},
  author={Young Woo Kim and Hee Eun Kang and Myung G. Lee and Se Jin Hwang and Sang Chan Kim and Chang Ho Lee and Sang -Geon Kim},
  journal={American journal of physiology. Gastrointestinal and liver physiology},
  year={2009},
  volume={296 2},
  pages={
          G372-81
        }
}
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… 
Pharmacokinetics of liquiritigenin and its two glucuronides, M1 and M2, in rats with acute hepatitis induced by d-galactosamine/lipopolysaccharide or CCl4
  • H. Kang, Y. Kim, +5 authors M. Lee
  • Biology, Medicine
    Xenobiotica; the fate of foreign compounds in biological systems
  • 2010
TLDR
Modification of oral dosage regimen of LQ may not be necessary in patients with acute hepatitis; but human studies are required.
HEPATOPROTECTIVE EFFECT OF GAMAVUTON-0 AGAINST D˗GALACTOSAMINE/LIPOPOLYSACCHARIDE-INDUCED FULMINANT HEPATIC FAILURE
TLDR
Results indicated that the GVT-0 mainly lower dose showed hepatoprotective action in rat model of fulminant  hepatitis induced by D-GalN/LPS is not via  antioxidant  properties  of  G VT-0, and further studies are necessary to explain the molecular mechanism.
Pharmacokinetic interaction between liquiritigenin (LQ) and DDB: increased glucuronidation of LQ in the liver possibly due to increased hepatic blood flow rate by DDB.
Pharmacokinetics and first-pass effects of liquiritigenin in rats: low bioavailability is primarily due to extensive gastrointestinal first-pass effect
  • H. Kang, Y. Cho, +4 authors M. Lee
  • Medicine, Biology
    Xenobiotica; the fate of foreign compounds in biological systems
  • 2009
TLDR
In vitro metabolism of liquiritigenin in S9 fractions of rat tissues showed that the liver and intestine were major tissues responsible for glucuronidation of liquspiritigenin, a candidate for inflammatory liver disease, and its two glucuronide conjugates, M1 and M2, were evaluated in rats.
HuangQin Decoction Attenuates CPT-11-Induced Gastrointestinal Toxicity by Regulating Bile Acids Metabolism Homeostasis
TLDR
The present study demonstrated for the first time that the precise interaction between HQD, CPT-11-induced intestinal toxicity and BAs’ homeostasis is demonstrated.
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References

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TLDR
In Eisai hyperbilirubinemic rats, which have a hereditary defect in the canalicular transport system for several organic anions, the biliary excretion clearance of M1, M2, M4 and M5 was markedly reduced, whereas that of M3 was comparable with that in control rats.
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The present article aims to review the up-to-date information on the studies of the first-pass metabolism, in particular glucuronidation, of flavonoids in the gastrointestinal tract and the liver, and also the isoformic enzymes involved in the metabolism and disposition of Flavonoids.
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TLDR
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  • Biology
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TLDR
Drug metabolism and microbial metabolism of green tea catechins in in vitro systems and in animals and in humans will be reviewed and the factors affecting their biotransformation and bioavailability are covered.
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TLDR
The roles of the rat small intestine in the glucuronidation and methylation of flavonoids as well as the role of the liver in sulfation, methylation and biliary excretion are demonstrated.
Effect of galactosamine-induced hepatic UDP-glucuronic acid depletion on acetaminophen elimination in rats. Dispositional differences between hepatically and extrahepatically formed glucuronides of acetaminophen and other chemicals.
TLDR
The effect of GAL-induced hepatic UDP-GA depletion was examined in bile duct-cannulated rats to determine the role of hepatic glucuronidation in the disposition of acetaminophen (AA).
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TLDR
The hypothesis that uridine prevents d ‐galactosamine hepatotoxicity not only by rescuing the hepatocyte in the late phases of the injury but also preventing TNF‐α release from Kupffer cells thereby blocking apoptosis that occurs early after d ‬galactOSamine treatment is supported.
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