〔Abstract〕 Objective To explore the molecular mechanism of fasudil-modified macrophages in the treatment of experimental allergic encephalomyelitis(EAE). Methods C57 BL/6 mice were induced by myelin oligodendrocyte glycoprotein(MOG) to establish an active immune EAE model. Peritoneal macrophages were prepared after 9 days of immunization and the mice were either unable to be treated with or without fasuldil for 72 h(control group and experimental group). Macrophages from the control group and the experimental group were transfused into EAE mice models, with each mouse containing 5×107cells. After treatment for 10 days,the changes of clinical behavior and body weight of mice in the control group and experimental group were analyzed. Macrophages in the two groups were isolated from the abdominal cavity and the ratio of M1 and M2 macrophages in the two groups was analyzed by flow cytometry. The expression of macrophage markers in M1 and M2 was analyzed by fluorescence quantitative PCR. The levels of interleukin-10(IL-10) and interleukin-12(IL-12) were analyzed by enzyme-linked immunosorbent assay(ELISA). Results The clinical symptom score of the experimental group was significantly lower than that of the control group(F=6.135,P<0.001). Compared with the control group, the weight loss of mice in the experimental group was less, and the difference was statistically significant(F=3.105,P=0.011). Compared with the control group, the M2-labeled arginase(Arg-1), YM-1, FIZZ and IL-10 cytokine levels in the observation group increased significantly, while the M1-labeled nitric oxide synthase(iNOS) and IL-12 cytokine levels decreased significantly(t=7.091,P<0.001;t=11.094,P<0.001;t=6.182,P<0.001;t=3.942,P<0.001;t=4.132,P<0.001;t=3.198,P<0.001). Compared with the control group, the proportion of macrophages in F4/80-CD206 increased significantly, while the proportion of macrophages in F4/80-CD16/32 decreased significantly(t=10.618,P<0.001;t=12.105,P<0.001). Conclusion Fasudil-modified macrophages can significantly improve the clinical symptoms of EAE mice, and its mechanism is mainly through improving the polarity of macrophages.