Davallialactone protects against acetaminophen overdose-induced liver injuries in mice

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dc.contributor.authorJung Ran Noh-
dc.contributor.authorYong Hoon Kim-
dc.contributor.authorJung Hwan Hwang-
dc.contributor.authorGil Tae Gang-
dc.contributor.authorKyoung Shim Kim-
dc.contributor.authorI K Lee-
dc.contributor.authorB S Yun-
dc.contributor.authorChul Ho Lee-
dc.date.accessioned2017-04-19T09:39:06Z-
dc.date.available2017-04-19T09:39:06Z-
dc.date.issued2013-
dc.identifier.issn0278-6915-
dc.identifier.uri10.1016/j.fct.2013.04.005ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11294-
dc.description.abstractOxidative stress is closely associated with acetaminophen (APAP)-induced toxicity. Davallialactone (DAVA), a hispidin analog derived from the mushroom Inonotus xeranticus, has antioxidant properties. This study evaluated whether DAVA plays protective roles against APAP hepatotoxicity in mice. Pretreatments with DAVA (10. mg/kg) prior to exposures of mice to a hepatotoxic dose of 600. mg/kg APAP significantly increased survival rate compared to APAP alone. To verify this effect, mice were treated with 400. mg/kg APAP 30. min after DAVA administration and were then sacrificed after 0.5, 1, 3, and 6. h. APAP alone caused severe liver injuries as characterized by increased plasma GOT and GPT levels, ATP and GSH depletion, and peroxynitrite and 4-HNE formations. These liver damages induced by APAP were significantly attenuated by DAVA pretreatments. The GSH/GSSG ratio nearly recovered to the levels observed in non-APAP-treated mice at 6. h after APAP treatment in DAVA-pretreated mice. Furthermore, while hepatic ROS levels were increased by APAP exposures, pretreatments with DAVA completely blocked ROS formation. In addition, APAP-induced sustained activations of JNK and ERK were remarkably reduced by DAVA pretreatment. In conclusion, these results suggest that DAVA plays protective roles against APAP-mediated hepatotoxicity through function as ROS scavenger.-
dc.publisherElsevier-
dc.titleDavallialactone protects against acetaminophen overdose-induced liver injuries in mice-
dc.title.alternativeDavallialactone protects against acetaminophen overdose-induced liver injuries in mice-
dc.typeArticle-
dc.citation.titleFood and Chemical Toxicology-
dc.citation.number1-
dc.citation.endPage21-
dc.citation.startPage14-
dc.citation.volume58-
dc.contributor.affiliatedAuthorJung Ran Noh-
dc.contributor.affiliatedAuthorYong Hoon Kim-
dc.contributor.affiliatedAuthorJung Hwan Hwang-
dc.contributor.affiliatedAuthorGil Tae Gang-
dc.contributor.affiliatedAuthorKyoung Shim Kim-
dc.contributor.affiliatedAuthorChul Ho Lee-
dc.contributor.alternativeName노정란-
dc.contributor.alternativeName김용훈-
dc.contributor.alternativeName황정환-
dc.contributor.alternativeName강길태-
dc.contributor.alternativeName김경심-
dc.contributor.alternativeName이인경-
dc.contributor.alternativeName윤봉식-
dc.contributor.alternativeName이철호-
dc.identifier.bibliographicCitationFood and Chemical Toxicology, vol. 58, no. 1, pp. 14-21-
dc.identifier.doi10.1016/j.fct.2013.04.005-
dc.subject.keywordAcetaminophen-
dc.subject.keywordDavallialactone-
dc.subject.keywordLiver-
dc.subject.keywordOxidative stress-
dc.subject.keywordToxicity-
dc.subject.localAcetaminophen-
dc.subject.localDavallialactone-
dc.subject.localdavallialactone-
dc.subject.localliver-
dc.subject.localLiver-
dc.subject.locallivers-
dc.subject.localOxidative stre-
dc.subject.localOxidative stress-
dc.subject.localOXIDATIVE STRESS-
dc.subject.localOxidative Stress-
dc.subject.localoxidative stress-
dc.subject.localtoxicity-
dc.subject.localToxicity-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
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