Objective To testify the link between the increase of inducible nitric oxide synthase (iNOS) and monocarboxylate transporter 1 (MCT1) expression in the M1 phenotype microglia under ischemic condition.   Methods  Photothrombosic ischemia stroke model was applied in 6 mice. BV2 cells were treated with low glucose medium contained 5mmol/L glucose for 2 hours. Immunofluorescent staining and Western blotting were used to check the responses from microglia in the mouse brains subjected to ischemia and BV2 cells were treated with low-glucose treatment. Application of RNA interference or plasmid transfection were used to regulate the MCT1 expression in BV2 cells.   Results  The expression levels of iNOS, MCT1 and arginase-1 (ARG1) increased in the ischemic side compared to the non-ischemic side of mice brain(P<0.01). In the BV2 cells exposed to low-glucose condition, iNOS and MCT1 levels increased(P<0.001), whereas ARG1 level decreased(P<0.01). RNA interference interfered the expression of MCT1 and then decreased the iNOS expression(P<0.01), while overexpression of MCT1 through plasmid transfection increased iNOS expression(P<0.01), while the ARG1 expressions in both conditions were not changed significantly.   Conclusion  After microglia polarized into inflammatory phenotype during ischemia period, iNOS production is related with MCT1 expression, and MCT1 is in the upstream of iNOS pathway.