Protective Effects of Salidroside against Acetaminophen-Induced Toxicity in Mice

The protective effect of salidroside (SDS) isolated from Rhodiola sachalinensis A. BOR. (Crassulaceae), was investigated in acetaminophen (APAP)-induced hepatic toxicity mouse model in comparison to N-acetylcysteine (NAC). Drug-induced hepatotoxicity was induced by an intraperitoneal (i.p.) injectio...

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Bibliographic Details
Published in:Biological & Pharmaceutical Bulletin 2008/08/01, Vol.31(8), pp.1523-1529
Main Authors: Wu, Yan-Ling, Piao, Dong-Ming, Han, Xue-Hua, Nan, Ji-Xing
Format: Article
Language:eng ; jpn
Subjects:
acetaminophen
Acetaminophen - antagonists & inhibitors
Acetaminophen - toxicity
Alanine Transaminase - blood
Analgesics, Non-Narcotic - antagonists & inhibitors
Analgesics, Non-Narcotic - toxicity
Animals
Aspartate Aminotransferases - blood
Caspase 3 - metabolism
Chemical and Drug Induced Liver Injury - enzymology
Chemical and Drug Induced Liver Injury - pathology
Chemical and Drug Induced Liver Injury - prevention & control
Crassulaceae
Glucosides - pharmacology
Glutathione - metabolism
hepatotoxicity
hypoxia inducible factor-1α
Hypoxia-Inducible Factor 1, alpha Subunit - biosynthesis
Hypoxia-Inducible Factor 1, alpha Subunit - genetics
Immunohistochemistry
Lipid Peroxidation - drug effects
Liver - drug effects
Liver - enzymology
Male
Malondialdehyde - metabolism
Mice
Mice, Inbred C57BL
Oxidative Stress - physiology
Phenols - pharmacology
Rhodiola - chemistry
salidroside
Tumor Necrosis Factor-alpha - blood
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Summary:The protective effect of salidroside (SDS) isolated from Rhodiola sachalinensis A. BOR. (Crassulaceae), was investigated in acetaminophen (APAP)-induced hepatic toxicity mouse model in comparison to N-acetylcysteine (NAC). Drug-induced hepatotoxicity was induced by an intraperitoneal (i.p.) injection of 300 mg/kg (sub-lethal dose) of APAP. SDS was given orally to mice at a dose of 50 or 100 mg/kg 2 h before the APAP administration in parallel with NAC. Mice were sacrificed 12 h after the APAP injection to determine aspartate aminotransferase (AST), alanine aminotransferase (ALT), and tumor necrosis factor-alpha (TNF-α) levels in serum and glutathione (GSH) depletion, malondialdehyde (MDA) accumulation, and caspase-3 expression in liver tissues. SDS significantly protected APAP-induced hepatotoxicity for SDS improved mouse survival rates better than NAC against a lethal dose of APAP and significantly blocked not only APAP-induced increases of AST, ALT, and TNF-α but also APAP-induced GSH depletion and MDA accumulation. Histopathological and immunohistochemical analyses also demonstrated that SDS 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 SDS protected liver tissue from the APAP-induced oxidative damage via preventing or alleviating intracellular GSH depletion and oxidation damage, which suggested that SDS would be a potential antidote against APAP-induced hepatotoxicity.
ISSN:0918-6158
1347-5215
DOI:10.1248/bpb.31.1523