The natural product fucoidan ameliorates hepatic ischemia-reperfusion injury in mice.

Fucoidan is a sulfated polysaccharide based predominantly on l-fucose, and has several biologic functions. Reactive oxygen species-mediated apoptosis and autophagy and release of related inflammatory factors have important roles in hepatic ischemia-reperfusion injury (IR). Here, the effect of fucoidan on hepatic IR was investigated. Mice were randomized into sham, IR, and fucoidan (20, 40mg/kg for 14days) groups. Samples were collected to assess biochemical indicators, hepatocyte damage and levels of proteins related to signaling pathways at different time points. Fucoidan had no effect on normal liver tissue, but inhibited the increases in alanine aminotransferase, aspartate transaminase, inflammatory factors, and the hepatocyte damage caused by IR. Also, apoptosis and autophagy via the activated JAK2/STAT1 pathway were attenuated by fucoidan to protect against hepatic injury. In conclusion, fucoidan ameliorates hepatic IR injury in mice via JAK2/STAT1-mediated apoptosis and autophagy. Inhibition of this pathway may be associated with reduced release of related inflammatory cytokines, especially interferon-γ.