Schisantherin A protects against liver ischemia-reperfusion injury via inhibition of mitogen-activated protein kinase pathway

- SchA exerts protective effects in hepatic I/R model.
- SchA ameliorated oxidative/nitrosative stress, inflammatory state, and cell apoptosis.
- SchA failed to induce cell autophagy.
- The underlying mechanism of SchA involves the inhibition of MAPK signaling pathway.

Schisantherin A (SchA) is a dibenzocyclooctadiene lignan isolated from the fruit of Schisandra sphenanthera. The role of SchA in liver injury induced by ischemia and reperfusion (I/R) has not yet been elucidated. The present study hypothesized the protective effects of SchA in hepatic I/R model. Either sham laparotomy or hepatic I/R was induced in C57BL/6 male mice after SchA or vehicle administration. Liver function, histological damage, oxidative/nitrosative stress, inflammatory infiltration, cytokine production, cell apoptosis, cell autophagy, and I/R-associated intracellular signaling pathway were assessed to evaluate the impact of SchA pretreatment on I/R-induced liver injury. After liver I/R injury, the mice pretreated with appropriate SchA displayed significantly preserved liver function, less histological damage, ameliorated oxidative/nitrosative stress, attenuated inflammatory state, and reduced cell apoptosis. However, no differences in the autophagic response were detected after SchA pretreatment. The underlying protective mechanism putatively involves the inhibition of mitogen-activated protein kinase (MAPK) signaling pathway. Based on the beneficial effects, SchA pretreatment may serve as a potential prophylactic measure to prevent liver I/R injury related to various clinical conditions.