Protective effect of forsythiaside A on lipopolysaccharide/d-galactosamine-induced liver injury

• Forsythiaside attenuated hepatic pathological damage and serum ALT, and AST levels induced by LPS/GalN.
• Forsythiaside inhibited NF-κB activation, serum TNF-α and hepatic TNF-α levels induced by LPS/GalN.
• Forsythiaside up-regulated the expression of Nrf2 and heme oxygenase-1.

Forsythiaside A, an active constituent isolated from air-dried fruits of Forsythia suspensa, has been reported to have multiple pharmacological activities including anti-inflammatory, anti-oxidant, and antioxidant activities. In the present study, the hepatoprotective effect of forsythiaside A was investigated in lipopolysaccharide (LPS)/d-galactosamine (GalN)-induced acute liver injury in mice. Mice acute liver injury model was induced by LPS (50 μg/kg)/GalN (800 mg/kg). Forsythiaside A was administrated 1 h prior to LPS/GalN exposure. The results showed that forsythiaside A attenuated hepatic pathological damage, malondialdehyde (MDA) content, and serum ALT, and AST levels induced by LPS/GalN. Moreover, forsythiaside A inhibited NF-κB activation, serum TNF-α and hepatic TNF-α levels induced by LPS/GalN. Furthermore, we found that forsythiaside A up-regulated the expression of Nrf2 and heme oxygenase-1. Our results showed that forsythiaside A protected against LPS/GalN-induced liver injury through activation of Nrf2 and inhibition of NF-κB activation.