Glycyrrhizin is the major active component extracted from licorice (
Glycyrrhiza glabra) roots, one of the most widely used herbal preparations for the treatment of liver disorders. This study evaluated the potential beneficial effect of glycyrrhizin in a mouse model of carbon tetrachloride (CCl
4)-induced liver injury. The mice were treated intraperitoneally with CCl
4 (0.5 ml/kg). They received glycyrrhizin (50, 100, 200, 400 mg/kg) 24 h and 0.5 h before and 4 h after administering CCl
4. The serum activities of aminotransferase and the hepatic level of malondialdehyde were significantly higher 24 h after the CCl
4 treatment, while the concentration of reduced glutathione was lower. These changes were attenuated by glycyrrhizin. CCl
4 increased the level of circulating tumor necrosis factor-α markedly, which was reduced by glycyrrhizin. The levels of hepatic inducible nitric oxide synthase, cyclooxygenase-2, and heme oxygenase-1 protein expression were markedly higher after the CCl
4 treatment. Glycyrrhizin diminished these alterations for inducible nitric oxide and cyclooxygenase-2 but the protein expression of heme oxygenase-1 was further elevated by the treatment of glycyrrhizin. CCl
4 increased the level of
tumor necrosis factor-α,
inducible nitric oxide synthase,
cyclooxygenase-2, and
heme oxygenase-1 mRNA expressions. The mRNA expression of
heme oxygenase-1 was augmented by the glycyrrhizin treatment, while glycyrrhizin attenuated the increase in
tumor necrosis factor-α,
inducible nitric oxide synthase, and
cyclooxygenase-2 mRNA expressions. These results suggest that glycyrrhizin alleviates CCl
4-induced liver injury, and this protection is likely due to the induction of heme oxygenase-1 and the downregulation of proinflammatory mediators.
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