Protective effect of baicalin against carbon tetrachloride-induced acute hepatic injury in mice.

This study examined the effects of baicalin, a bioactive flavonoid isolated from Scutellariae Radix, on carbon tetrachloride (CCl(4))-induced liver injury. Mice were treated intraperitoneally with 0.5 ml/kg CCl(4) and different groups of animals received 25, 50, 100, and 200 mg/kg baicalin. At 24 h after the CCl(4) treatment, the level of serum aminotransferases and lipid peroxidation was significantly elevated, whereas the hepatic glutathione content was decreased. These changes were attenuated by baicalin. The histological studies showed that baicalin inhibited the portal inflammation, centrizonal necrosis, and Kupffer cell hyperplasia, which are the three most common characteristics of CCl(4)-induced liver damage. The serum level and mRNA expression of tumor necrosis factor-alpha were markedly increased by the CCl(4) treatment but suppressed by baicalin. The mRNA and protein expression levels of inducible nitric oxide synthase and heme oxygenase-1 increased significantly at 24 h after the CCl(4) treatment. Baicalin attenuated the increase in the protein and gene expression of inducible nitric oxide synthase but augmented the increase in those of heme oxygenase-1. These findings suggest that baicalin protects hepatocytes from the oxidative damage caused by CCl(4), and this protection is likely due to the induction of HO-1 expression and the inhibition of the proinflammatory mediators.