Schisandrin B modulates the ischemia-reperfusion induced changes in non-enzymatic antioxidant levels in isolated-perfused rat hearts

Isolated Langendorff-perfused rat hearts were subjected to a fixed period of ischemia followed by increasing periods of reperfusion for investigating the changes in the extent of ischemia-reperfusion (IR) injury and tissue levels of non-enzymatic antioxidants. Effects of schisandrin B (Sch B) and (±) α-lipoic acid (LA) pretreatment were also examined. A 40-min of ischemia (40-I) followed by 20- or 40-min of reperfusion (20-R or 40-R) caused sustainable tissue damage in isolated hearts, as indicated by the increased extent of lactate dehydrogenase (LDH) leakage and impaired contractile force. The myocardial IR injury was associated with a marked decrease in tissue ascorbic acid (V_c) level. However, myocardial reduced glutathione (GSH) and α-tocopherol (V_E) levels remained relatively unchanged except under a more severe IR condition (40-I, 40-R). Pretreating rats with Sch B or LA at a daily dose of 1.2 mmol/kg for 3 days protected against IR injury in isolated hearts to varying degrees. While only Sch B pretreatment could improve the recovery of contractile force, LA pretreatment produced a better inhibitory effect on LDH leakage. The protection against IR injury was associated with significant increases in myocardial V_E and V_c levels in both Sch B and LA pretreated hearts. The ensemble of results suggests that the cardioprotection afforded by Sch B or LA pretreatment may at least in part be attributed to the modulation on the interplay among non-enzymatic antioxidants under oxidative stress induced by IR.