AimTo study the recombinant human tumor necrosis factor-α receptorⅡ∶IgG Fc fusion protein （rhTNFR∶Fc）, ischemic postcondition （postcon）, and both combination on the prevention of myocardium ischemia/reperfusion injury.Methods48 SD rats were randomly divided into four groups， all rats were subjected to 1 h of LAD occlusion followed by 6 h of reperfusion.In Control group, no interventions were applied; in rhTNFR∶Fc group, rhTNFR∶Fc solution (2 mL/kg, 1 g/L) was administered intravenouslly at 30 min after ischemia; in postcon group∶ three cycles of 10 s of reperfusion and 10 s of reocclusion was applied immediately at the onset of reperfusion; in combination therapy group∶rhTNFR∶Fc solution (2 mL/kg, 1 g/L) was administered intravenouslly at 30 min after ischemia, and three cycles of 10 s of reperfusion and 10 s of reocclusion was applied immediately at the onset of reperfusion.We measured plasma lactate dehydrogenase (LDH), creatine kinase isoenzyme MB (CK-MB), tumor necrosis factor-α(TNF-α) levels at different time after reperfusion and examined ischemic and infarct area, apoptosis, the activity of Caspase-3, Bcl-2 at risk myocardium at the end of reperfusion.ResultsrhTNFR∶Fc, ischemic postcondition, both combination reduced the plasma LDH, CK-MB, TNF-α levels (at 30 min, 1 h, 3 h, 6 h after reperfusion), infarct area, apoptotic myocytes, Caspase-3 activity, increased Bcl-2 activity when compared with controls(P<0.01). Ischemic postcondition reduced the plasma TNF-α more significantly than rhTNFR∶Fc at 30 min and 1 h after reperfusion (P<0.01).However, at 3 h and 6 h after reperfusion, rhTNFR∶Fc reduced the plasma TNF-α more significantly (P<0.01).ConclusionBoth rhTNFR∶Fc and ischemic postcondition can inhibit TNF-α activity, attenuate myocyte apoptosis, and there is an additive effect when used in combination.