Although it has been proved that remote limb preconditioning (RPC) can exert neurological protection effects after ischemic cerebral stroke (ICS), the underlying mechanisms of RPC still need to be elucidated for its better transformation to clinical application. Lipocalin-2 (LCN2) was upregulated after cerebral ischemia and mediated reperfusion injury in the models of ischemic stroke. So here, we investigated that whether RPC could downregulate the levels of LCN2 protein and its receptor resulting from cerebral ischemia reperfusion (I/R) injury. The results showed that RPC could decrease the expression of LCN2 protein, but having no obvious effects on its receptor except the time point of 72 h after cerebral ischemia. Furthermore, we observed the downregulation of Bim after RPC in the course of ICS.