Protective Effect of Linarin Against β-Galactosamine and Lipopolysaccharide-Induced Hepatic Failure

Linarin is a natural occurring flavanol glycoside derived from Chrysanthemum indicum, which exerts remarkable anti-inflammatory, antioxidant and immunomodulatory properties. Fulminant hepatic failure (FHF) is a serious clinical syndrome that results in massive inflammation and hepatocyte death. Apoptosis is an important cellular pathological process in d-galactosamine (GalN)/lipopolysaccharide (LPS)-induced liver injury, and regulation of liver apoptosis might be an effective therapeutic method for FHF. In this study, we investigated the hepatoprotective effect of linarin against GalN/LPS-induced hepatic failure. Mice were given an oral injection of linarin (50 mg/kg; dissolved in 10% tween 80) 1h before receiving GalN (800 mg/kg)/LPS (40 µg/kg). Linarin treatment reversed the lethality induced by GalN/LPS. The level of serum alanine aminotransferase activity significantly elevated 6 h after GalN/LPS injection, which was inhibited by linarin. After 6 h of GalN/LPS injection, the levels of serum tumor necrosis factor (TNF)-α, interleukin (IL)-6, and hepatic TNF-α, IL-6 and interferon-β mRNA expression significantly increased. These increases were attenuated by linarin. Linarin attenuated the GalN/LPS-induced increases of caspase-3 activity, and number of TUNEL-positive cells. Our results suggest that linarin alleviates GalN/LPS-induced liver injury and this protection might be due to its anti-inflammatory and anti-apoptotic activities.