Abstract
The aim of this study was to investigate the mechanism and nature of the protective effect of Inula britannica flower flavonoids (IBFF) on antioxidants and the inhibition of inflammation in liver injury. Liver injury was induced in a mouse model by intraperitoneal injection of D-Galactosamine (D-Gal; 850 mg/kg) and IBFF was administered orally at 125, 250 or 500 mg/kg once a day for 7 days. The results revealed that IBFF reversed the increases in serum aminotransferase levels and lipid peroxidation and also reversed the decreases in hepatic glutathione content. IBFF attenuated the D-Gal-induced increases in tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) mRNA and protein levels in the liver. Our data suggest that IBFF ameliorates D-Gal-induced acute liver injury and that this protection may be due to its antioxidative and anti-inflammatory activities.
MeSH terms
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Administration, Oral
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Alanine Transaminase / blood
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Animals
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Anti-Inflammatory Agents / isolation & purification
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Anti-Inflammatory Agents / therapeutic use*
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Antioxidants / isolation & purification
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Antioxidants / therapeutic use*
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Aspartate Aminotransferases / blood
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Chemical and Drug Induced Liver Injury / etiology
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Chemical and Drug Induced Liver Injury / metabolism
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Chemical and Drug Induced Liver Injury / prevention & control*
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Cyclooxygenase 2 / genetics
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Cyclooxygenase 2 / metabolism
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Flavonoids / isolation & purification
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Flavonoids / therapeutic use*
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Flowers / chemistry
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Galactosamine / toxicity
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Glutathione / metabolism
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Inula / chemistry*
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Lipid Peroxidation
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Male
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Mice
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Nitric Oxide Synthase Type II / genetics
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Nitric Oxide Synthase Type II / metabolism
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RNA, Messenger / metabolism
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Tumor Necrosis Factor-alpha / genetics
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Tumor Necrosis Factor-alpha / metabolism
Substances
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Anti-Inflammatory Agents
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Antioxidants
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Flavonoids
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RNA, Messenger
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Tumor Necrosis Factor-alpha
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Galactosamine
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Nitric Oxide Synthase Type II
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Cyclooxygenase 2
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Aspartate Aminotransferases
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Alanine Transaminase
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Glutathione