Objective      To explore the effect of 17β-estradiol on Rho-kinase expression in the central nervous system (CNS) of experimental autoimmune encephalomyelitis (EAE) rats and related mechanism.       Methods      Seventy-five female Wistar rats were randomly divided into a normal group

an EAE group

a DMSO control group

an E2 group

and an E2+ICI group. Except for the rats of the normal group

the rats of the other 4 groups were first given ovariectomy to construct EAE rat models. The rats of the E2 group were treated with once daily s.c. injection of 17β-estradiol [20 μg/(kg·d)] for 10 d

and the rats of the E2+ICI group were treated with a nuclear estrogen receptor antagonist ICI 182780 [5 mg/(kg·d)] before 17β-estradiol injection. Neurological function scores were recorded and compared among the groups. HE staining was applied for pathological evaluation. The expression of Rho-kinase in each group was examined by immunohistochemistry and Western blotting.       Results      The treatment with 17β-estradiol resulted in a delay in EAE onset (P0.05) as well as a lower neurological function score (P0.05) in the E2 group as compared with those in the EAE group and the DMSO control group. The infiltration of inflammatory cells was alleviated in the E2 group showed by H-E staining. Immunohistochemistry result showed that the number of Rho-kinase-positive cells in the E2 group (8.36±1.57) was significantly lower than that in the EAE group (17.55±1.70

P0.01). Western blotting results showed the expression of Rho-kinase protein in the E2 group (0.833±0.022) was significantly lower than that in the EAE group (1.013±0.06

P0.05). The number of Rho-kinase-positive cells (18.90±2.39) and Rho-kinase protein expression (1.141±0.046) in the E2+ICI group were significantly higher than those in the E2 group (P0.05).       Conclusion      17β-estradiol can inhibit the expression of Rho-kinase in EAE rats by classical nuclear estrogen receptor pathway.