Progranulin (PGRN), a cysteine-rich secretory protein, is implicated in neuronal protection. In the central nervous system, it has been reported that PGRN protects against neuroinflammation after cerebral ischemia. On the other hand, granulin (GRN), which is cleaved from PGRN by neutrophil elastase, exerts pro-inflammatory effects. However, roles of PGRN and GRN after cerebral ischemia have not been fully determined. In this study, we examined time-course of changes in the levels of PGRN and GRN and their cellular sources after cerebral ischemia. A rat microsphere-embolism (ME) model and primary cultured microglia isolated from cerebral cortex were used. Protein and mRNA levels of PGRN were increased in the ischemic region of cerebral cortex on day 3 after ME. Furthermore, expression of PGRN was increased in activated microglia after ME. Elastase activity in cerebral cortex was increased on day 1 after ME. GRN protein was increased on day 1 after ME. These results suggest that increased elastase activity causes cleavage of PGRN, and then GRN may promote inflammatory responses after ischemia. Thus, the changes in the levels of PGRN and GRN might contribute to pathological alterations in ischemic disorders.