Davallialactone protects against acetaminophen overdose-induced liver injuries in mice

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Title
Davallialactone protects against acetaminophen overdose-induced liver injuries in mice
Author(s)
Jung Ran NohYong Hoon KimJung Hwan Hwang; Gil Tae Gang; Kyoung Shim Kim; I K Lee; B S Yun; Chul Ho Lee
Bibliographic Citation
Food and Chemical Toxicology, vol. 58, no. 1, pp. 14-21
Publication Year
2013
Abstract
Oxidative 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.
Keyword
AcetaminophenDavallialactoneLiverOxidative stressToxicity
ISSN
0278-6915
Publisher
Elsevier
DOI
http://dx.doi.org/10.1016/j.fct.2013.04.005
Type
Article
Appears in Collections:
Ochang Branch Institute > Division of Bioinfrastructure > Laboratory Animal Resource Center > 1. Journal Articles
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