Aim To investigate the effects of minocycline postconditioning on myocardial ischemia-reperfusion injury in rats and its possible mechanism. Methods Ninety-six male Wistar rats were randomly divided into four groups：sham-operation group，ischemia-reperfusion（IR） group，low-dose minocycline （3 mg/kg） group and high-dose minocycline （10 mg/kg） group. The rat model of myocardial IR was established by occlusion of the left anterior descending coronary artery for 45 min and reperfusion for 2 hours or 24 hours. After 2 h reperfusion,myocardial area at risk and infarct size were evaluated the amount of TNF-α,IL-1β in serum and myocardium and cardiac MPO activity were assayed myocardial apoptosis index（AI） and the myocardial tissue morphology were detected. The parameters of haemodynamics and myocardial area at risk and infarct size were evaluated 24 h after reperfusion. Results Compared with IR group,both low-dose and high-dose minocycline reduced LVEDP,enhanced HR,LVSP and±dp/dt_max,lowered the amount of TNF-α,IL-1β in serum and myocardium,cardiac MPO activity,and AI （P<0.05 or P<0.01）. Conclusion Minocycline postconditioning may ameliorate heart functions and decrease the infarct size and myocardial apoptosis induced by myocardial IR injury in vivo rats,and the protective effect may be related to interfering with the local and systemic inflammatory reactions.