Objective To observe the effect of remote ischemic postconditioning (RIPostC) on macrophage inflammatory protein-1alpha (MIP-1α) expression induced by cerebral ischemia-reperfusion injury in rats, and preliminary investigate the effect of RIPostC on inflammatory response. Methods A total of 77 male Sprague-Dawley (SD) rats (280-310g) were randomly divided into 7 groups: (1) Sham group (S); (2) I/R 8 h group (I8); (3) I/R RIPostC 8 h group (R8); (4) I/R 24 h group (I24); (5) I/R RIPostC 24 h group (R24); (6) I/R 72 h group (I72); (7) I/R RIPostC 72 h group (R72). In the I/R groups, transient middle cerebral artery occlusion (MCAO) models were induced; In the I/R RIPostC groups, limb RIPostC was carried out by three cycles of 10 min occlusion/10 min release of the bilateral femoral artery using clamps immediately after reperfusion. Real-time quantitative PCR (QTR-PCR), western blot and immunofluorescence staining were used to observe the expression levels of MIP-1α. Results (1) The results of QRT-PCR demonstrated that the mRNA expression of MIP-1α were increased in both I/R and I/R R groups. I8, R8 and R24 groups were significantly increased (P<0.05). (2) Western blot showed that, compared with S group, the protein expression of MIP-1α were increased in both I/R and I/R R groups. I24, I72 groups were significantly increased (P<0.05). Compared with I/R group, the protein expression of MIP-1α were reduced in R24 and R72 groups, which R72 group was significantly decreased, with statistical significance (P<0.05). (3) The immunofluorescence results verify the conclusions of the Western blot. Conclusion MIP-1α involved in the inflammatory response induced by cerebral ischemic-reperfusion injury in rats, and remote ischemic postconditioning probably reduce inflammatory response to protect brain followed ischemic-reperfusion injury.