Hepatoprotective effects of 18β-glycyrrhetinic acid on carbon tetrachloride-induced liver injury: inhibition of cytochrome P450 2E1 expression

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dc.contributor.authorH G Jeong-
dc.contributor.authorH J You-
dc.contributor.authorS J Park-
dc.contributor.authorA R Moon-
dc.contributor.authorY C Chung-
dc.contributor.authorS K Kang-
dc.contributor.authorHyo Kon Chun-
dc.date.accessioned2017-04-19T08:59:20Z-
dc.date.available2017-04-19T08:59:20Z-
dc.date.issued2002-
dc.identifier.issn10436618-
dc.identifier.uri10.1016/S1043-6618(02)00121-4ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/5946-
dc.description.abstractThe protective effects of 18beta-glycyrrhetinic acid (GA), the aglycone of glycyrrhizin (GL) derived from licorice, on carbon tetrachloride-induced hepatotoxicity and the possible mechanisms involved in this protection were investigated in mice. Pretreatment with GA prior to the administration of carbon tetrachloride significantly prevented an increase in serum alanine, aspartate aminotransferase activity and hepatic lipid peroxidation in a dose-dependent manner. In addition, pretreatment with GA also significantly prevented the depletion of glutathione (GSH) content in the livers of carbon tetrachloride-intoxicated mice. However, reduced hepatic GSH levels and glutathione-S-transferase activities were unaffected by treatment with GA alone. Carbon tetrachloride-induced hepatotoxicity was also prevented, as indicated by a liver histopathologic study. The effects of GA on the cytochrome P450 (P450) 2E1, the major isozyme involved in carbon tetrachloride bioactivation, were also investigated. Treatment of mice with GA resulted in a significant decrease of the P450 2E1-dependent hydroxylation of p-nitrophenol and aniline in a dose-dependent manner. Consistent with these observations, the P450 2E1 expressions were also decreased, as determined by immunoblot analysis. GA also showed antioxidant effects upon FeCl(2)-ascorbate-induced lipid peroxidation in mice liver homogenate and upon superoxide radical scavenging activity. These results show that protective effects of GA against the carbon tetrachloride-induced hepatotoxicity may be due to its ability to block the bioactivation of carbon tetrachloride, primarily by inhibiting the expression and activity of P450 2E1, and its free radical scavenging effects.-
dc.publisherElsevier-
dc.titleHepatoprotective effects of 18β-glycyrrhetinic acid on carbon tetrachloride-induced liver injury: inhibition of cytochrome P450 2E1 expression-
dc.title.alternativeHepatoprotective effects of 18beta-glycyrrhetinic acid on carbon tetrachloride-induced liver injury: inhibition of cytochrome P450 2E1 expression-
dc.typeArticle-
dc.citation.titlePharmacological Research-
dc.citation.number3-
dc.citation.endPage227-
dc.citation.startPage221-
dc.citation.volume46-
dc.contributor.affiliatedAuthorHyo Kon Chun-
dc.contributor.alternativeName정혜광-
dc.contributor.alternativeName유호진-
dc.contributor.alternativeName박승준-
dc.contributor.alternativeName문애란-
dc.contributor.alternativeName정영철-
dc.contributor.alternativeName강신근-
dc.contributor.alternativeName전효곤-
dc.identifier.bibliographicCitationPharmacological Research, vol. 46, no. 3, pp. 221-227-
dc.identifier.doi10.1016/S1043-6618(02)00121-4-
dc.subject.keyword18β-glycyrrhetinic acid-
dc.subject.keywordAntioxidant-
dc.subject.keywordCarbon tetrachloride-
dc.subject.keywordCytochrome P450 2E1-
dc.subject.keywordHepatoprotective effects-
dc.subject.local18β-glycyrrhetinic acid-
dc.subject.localAntioxidant-
dc.subject.localCarbon tetrachloride-
dc.subject.localCytochrome P450 2E1-
dc.subject.localHepatoprotective effects-
dc.subject.localHepatoprotective effect-
dc.description.journalClassY-
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Division of Bio Technology Innovation > SME Support Center > 1. Journal Articles
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