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Our previous report indicates that hepatic ischemia reperfusion (I/R) injury related to abnormal increased leukotriene (LT) C4 production.Here we investigated mechanism underlying ischemic preconditioning (IP) effects on the LTC4 production in hepatic I/R injury rats.Adult male SD rats were randomly divided into sham, I/R and IP groups.Rat liver was subjected to 1 h of partial hepatic ischemia followed by 5 h of reperfusion with saline administered intravenously.The protein expressions of the leukotriene C4 synthase (LTC4S) was detected with western blotting;the LTC4 synthesis enzymes activities and LTC4 content were measured by RPHPLC.Serum NO2-and liver tissue GSH were also examined by biochemical methods.We noted that IP markedly decreased LTC4 content and inhibited LTC4S protein expression and the LTC4 synthesis enzymes activities in rat liver when compared with I/R group (P<0.05).The decline in serum NO2-(P<0.05) and the elevation in hepatic tissue GSH (P<0.05) in IP groups were also observed.The LTC4S positive expressions on hepatocytes and sinusoidal endothelial cells in IP group were significantly lower than that in I/R group.These findings firstly demonstrate that the reduced LTC4 production by IP treatment during hepatic I/R injury could be partially resulted from the down-regulation of LTC4S protein expressions and the depression of LTC4 synthesis enzymes activities,which may involve its reducing NO and stabilizing redox state during hepatic I/R in rats.