To explore a model of necroptosis in brain microvascular endothelial cells (BMECs) by mimic ischemia-reperfusion injury combined with z-VAD-FMK (Benzyloxyearbonyl-Val-Ala-Asp-fluoromethylketone， z-VAD-FMK). Methods:First， primary rat BMECs were cultured in oxygen-glucose deprivation (OGD) and reintroduction conditions for various time points to screen a time of mimic ischemia-reperfusion injury. Then， z-VAD-FMK， the casepase inhibitor， was administrated at 20 μmol/L concentration on the ischemia-reperfusion injured BMECs. The cell activity was detected by CCK-8. The ultra-stucture was observed using the transmission electron microscope. The death mode of BMECs was detected using cell ultrastructure; Annexin V-FIT C/PI (propidium iodide) double staining to detect the type of cell death. Results:OGD 2 h and reintroduction 8 h was determined to be the time point of mimic ischemia-reperfusion injury. After z-VAD-FMK was administrated on ischemia-reperfusion injuried BMECs， the cells viability didn’t change significantly. The necroptosis characteristic was presented under transmission electron microscope. The flowcytometry results showed that ratio of cells in each quadrant had no significant change. However， Nec-1， a specific inhibitor of necroptosis， could significantly decrease the ratio of cells in quadrant Q2， suggesting that intervention of z-VAD-FMK inhibited the late apoptosis and induced necroptosis occurrence. Conclusion:The necroptosis may be induced by z-VAD-FMK in ischemia-reperfusion injured BMECs， which provides the cell experimental model for researching necroptosis mechanism in the ischemic stroke in the future.