Background: Baicalin (BA) exhibits an anti-inflammatory effect in vivo and in vitro and is used to treat chronic hepatitis. However, the mechanism by which BA exerts the liver-protective effect remains largely unknown.
Aims: The present study reports that BA inhibits cytokine production and hepatocyte apoptosis to protect mice from liver injury induced by concanavalin A (Con A), a T-cell-dependent liver injury model.
Results: Con A injection of mice induced severe immune responses and extensive hepatocellular apoptosis within 24 h. Pretreatment of 200 or 100 mg/kg BA markedly reduced serum aminotransferase activities, protected hepatoycte apoptosis and reduced the increase of plasma cytokine levels, including tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and interleukin-6 (IL-6). Furthermore, BA pretreatment decreased tissue myeloperoxidase activity and lipid peroxidation, but increased the superoxide dismutase level. In vitro studies indicated that the beneficial effect of BA was associated with reduced cytokine production from lymphocytes and reduced TNF-alpha-induced hepatocyte apoptosis.
Conclusion: These results suggest that BA has therapeutic potential for T-cell-mediated liver injury.