Background　Reperfusion of tissues subjected to prolonged ischaemia can results in ischemia/reperfusion(I/R）injury. It has been shown that ischemic pre-and post-conditioning can reduce I/R injury about 75%.　Objective　To review molecular mechanisms of ischaemic pre-and post-conditioning attenuating I/R injury.　Content　The molecular mechanisms of ischaemic pre-and post-conditioning attenuating I/R injury involve the activation of surface G-protein-coupled receptors for adenosine, bradykinin, opioids, and cannabinoids. These in turn stimulate growth receptors which then trigger the activation of cytoprotective pathways resulting in a reduction in apoptosis via the mitogen-activated protein kinase(MEK）/extracellular-signal regulated kinase 1/2 (ERK1/2) route and a reduction in opening of mitochondrial permeability transition pores via the phosphatidylinositol 3-kinase pathway. Opening of mitochondrial permeability transition pores(mPTP) can cause cell death. The recent studies indicate that activated surface tumor necrosis factor-α receptors also contribute to cytoprotection by activating the Janus kinase and the signal transducer and activating factor of transcription-3 pathway.　Trend　The studies regarding molecular mechanisms of ischaemic pre-and post-conditioning attenuating I/R injury is still ongoing. It is hope that with the better understanding of these interventional strategies, possible translation into meaningful clinical therapies will be developed.