Protective effects of sea buckthorn polysaccharide extracts on LPS/D-Gal N-induced liver injury in mice and modulation on TLR4,SOCS3 expression

Objective: To study the protective effects of sea buckthorn polysaccharide extracts on lipopolysaccharide( LPS) /Dgalactosa mine( D-Gal N)-induced liver injury in mice and investigate the regulation on hepatic TLR4 and SOCS3 expression. Methods: C57 BL /6 male mice were randomly divided into six groups: control group,model group,dexamethasone positive control group,low,medium and high dose group of sea buckthorn polysaccharide. Mice in the sea buckthorn polysaccharides low,medium and high dose group were gavaged with 50,100 and 200 mg/kg sea buckthorn polysaccharide extracts for 14 days respectively. Acute liver injury model were established by intraperitoneal injection of LPS( 10 μg/kg) and D-Gal N( 700 mg/kg). The mice in the dexamethasone positive control group were intraperitoneally injected with dexamethasone( 10 mg/kg) before model establishment. Serum and liver samples were collected after model establishment for 4 h. Serum levels of ALT and AST were detected. Histological changes of liver tissue were observed by HE staining. Hepatic expression of TLR4 and SOCS3 was detected by Western blot. Results: Sea buckthorn polysaccharide significantly inhibited LPS/D-Gal N-induced elevation in serum levels of ALT and AST. It also alleviated liver cell injury and inflammatory infiltration. Western blot results showed that sea buckthorn polysaccharide inhibited LPS/D-Gal N-induced TLR4 expression. SOCS3 expression was not dramatically influenced by sea buckthorn polysaccharide supplementation. Conclusion: Sea buckthorn polysaccharide protects against LPS/D-Gal N-induced liver injury. This protective effects may be achieved by inhibiting the expression of TLR4 but not associated with modulation on SOCS3 expression.