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We tested the effectiveness of ischemic postconditioning (iPoC) in mitigating ischemia-reperfusion (I/R) injury of liver and the mechanism involves inhibiting the opening of the mitochondrial permeability transition pore (mPTP).iPoC, performed by three cycles of 1 min I/R of the liver, was tested on a partial liver I/R model on rats. The serum alanine transaminase levels, terminal deoxynucleotidyl transferase dUTP nick-end labeling staining, cytochrome c release, the formation of 4-hydroxy-2-nonnenal-modified proteins, and mitochondrial membrane potential (Δψm) were measured. Atractyloside (ATR) and NIM811, which modify the opening of mPTP, were administered in selected groups.iPoC, and NIM811, diminished the elevation of serum alanine transaminase level after I/R injury (174.0±28.3 U/L for iPoC; 94.3±25.4 U/L for control+NIM811) when compared with others (416.3±16.7 U/L for control, 557.0±86.7 U/L for iPoC+ATR, P<0.05). The expressions of cytosolic cytochrome c after I/R injury were decreased in iPoC and control+NIM811 groups when compared with others. After I/R, the apoptosis and the 4-hydroxy-2-nonnenal-modified proteins were attenuated in iPoC group when compared (apoptotic counts/50 HPF: 723.3±98.7 for iPoC, 1274±201.2 for control, 1057.6±39 for iPoC+ATR, P<0.05). The Δψm measured by flow cytometry was better preserved in iPoC and NIM811 groups.iPoC attenuated cell deaths after I/R injury of liver. The protective effects were negated by the addition of ATR—a mPTP opener—and mimicked by injection of NIM811—a mPTP opening inhibitor. The study indicated iPoC conferred protection by modulating mPTP.