Acanthoic acid, a diterpene in Acanthopanax koreanum, protects acetaminophen-induced hepatic toxicity in mice
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- Acanthoic acid, a diterpene in Acanthopanax koreanum, protects acetaminophen-induced hepatic toxicity in mice
- Y L Wu; Y Z Jiang; X J Jin; L H Lian; J Y Piao; Y Wan; H R Jin; Jung Joon Lee; J X Nan
- Bibliographic Citation
- Phytomedicine, vol. 17, no. 6, pp. 475-479
- Publication Year
- The protective effect of a diterpenoid acanthoic acid (AA) isolated from Acanthopanax koreanum Nakai was investigated in acetaminophen (APAP)-induced hepatic toxicity. Drug-induced hepatotoxicity induced by an intraperitoneal (i.p.) injection of 300 mg/kg (sub-lethal dose) of APAP. Pretreatment with AA (50 and 100 mg/kg) orally 2 h before the APAP administration attenuated the APAP-induced acute increase in serum aspartate aminotransferase (AST), and alanine aminotransferase (ALT) activites, replenished the depleted hepatic glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) activities, decreased malondialdehyde (MDA) level and considerably reduced the histopathological alterations in a manner similar to silymarin (Sily). Immunohistochemical analyses also demonstrated that AA could reduce the appearance of necrosis regions as well as caspase-3 and hypoxia inducible factor-1α (HIF-1α) expression in liver tissue. Our results indicated that AA protected liver tissue from the oxidative stress elicites by APAP-induced liver damage and suggestes that the hepatic protection mechanism of AA would relate to antioxidation and hypoxia factor on APAP-induced hepatotoxicity.
- Acanthoic acid; Acanthopanax koreanum; Acetaminophen; Antioxidation; Hepatotoxicity; Hypoxia inducible factor-1α
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