Objective To explore whether macrophage migration inhibitor factor (MIF)can protect human bone microvascular endothelial cells (HBMECs)from glucocorticoid-induced damage.Methods HUVECs were isolated from human femoral head.After HUVECs were cultured and identified,we constructed the ECs damage model with high-dose hydrocortisone.The cells were randomly divided into blank control group,low-dose MIF group,high-dose MIF group with corresponding treatment.Cell activity was detected by AlamarBlue in each group. The number of viable cells was detected in Live/Dead staining.The cell morphology was observed after cytoskeleton staining.Cell migration ability was compared by scratch test and the level of VEGF expression was detected by ELISA.Results Cell model was successfully constructed.The activity of cells in high-dose MIF group (178.3± 15.2)% was significantly higher than that in the control group (100±8.4)% and low-dose MIF group (149.1± 13.8)% (P<0.05).The number of viable cells in high-dose MIF group (139.5±14.3)% was higher than that in low-dose MIF group (121.3±12.9)% while the two groups had more viable cells than the control group (100± 8.4)% (P<0.05).The scratch test results indicated that cell migration ability in high-dose group was the strongest and the scratch disappeared at 24 hours after scratching.The expression of VEGF at 24 hours after intervention was (170±15.7)pg/mL in normal group,(328±25.3)pg/mL in low-dose group and (405±31.2)pg/mL in high-dose group.VEGF level was lower in low-dose group than in high-dose group (P<0.05),but higher than the normal group (P<0.01).Conclusion MIF can promote the proliferation and migration of ECs in a dose-dependent manner and upregulate the expression of VEGF.MIF can improve ECs damage induced by high-dose glucocorticoid.