Proinflammatory cytokines and chemokines are quickly upregulated in response to ischemia/reperfusion (I/R) injury; however, the relationship between I/R-induced oxidative stress and cytokine/chemokine expression has not been elucidated. We investigated the temporal profile of cytokine and chemokine gene expression in transient focal cerebral ischemia using complementary DNA array technology. Among 96 genes studied, 10, 4, 11, and 5 genes were increased at 6, 12, 24, and 72 h of reperfusion, respectively, whereas, 4, 11, 8, and 21 genes, respectively, were decreased. To clarify the relationship between chemokines and oxidative stress, we compared the gene and protein expression of monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein-1α (MIP-1α) in wild-type (WT) mice and copper/zinc-superoxide dismutase (SOD1) transgenic (Tg) mice. Monocyte chemoattractant protein-1 and MIP-1α mRNA were significantly upregulated at 6 to 12 h of reperfusion. In the SOD1 Tg mice, however, MCP-1 and MIP-1α mRNA expression was significantly decreased 12 h postinsult. In the WT mice, MCP-1 and MIP-1α protein expression peaked 24 h after onset of reperfusion determined by immunohistochemistry. In the SOD1 Tg mice, MCP-1 and MIP-1α immunopositive cells were reduced, as were concentrations of these proteins (measured by enzyme-linked immunosorbent assay) at 24 h of reperfusion. Our results suggest that MCP-1 and MIP-1α expression is influenced by I/R-induced oxidative stress after transient focal stroke.