Objective To investigate the mechanism of protective effects of 17-β estradiol on the experimental model of spinal cord injury (SCI) rats.Methods First,the primary astrocytes were cultured and identified.When the third generation astrocytes were cultured,they were induced by H202 whose concentrations were established by the method of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT).The cells were randomly divided into five groups:control group; the group of treatment with 400 μmol/L H2O2 for 24 hours; the group of treatment with 20 nmol/L estrogen for 2 hours prior to exposure to 400 μmol/L H2O2 for 24 hours; the group of treatment with 20 nmol/L estrogen for 26 hours and the group of treatment with dimethyl sulfoxide for 26 hours.The proteins which were extracted from these cells after treatments with H2O2 for 24 hours were detected by Western blotting.Results The absorbances of the astrocytes of treatments with H2O2 were reduced( q' =-11.45,P =0.001 ).But exposure to estrogen prior to exposure to H2O2 provided partial restoration of the absorbances (q' =7.025,P =0.0025 ).The absorbances of the astrocytes among different groups showed significant differences( F =69.69,P =0.0025 ).The results suggested that estrogen might increase the cell viability in astrocytes.Compared with the group of treatment cells with H2O2,treatment cells with 17-β estradiol prior to H2O2 exposure down-regulated the expressions of both phosphatase and tensin homologue deleted on chromosome 10 ( PTEN ) ( F =290.003,P =0.001 ) and caspase-3 ( F =46.158,P =0.023 ).And,17-β estradiol treatment of cells increased the levels of p-Akt ( F =49.173,P =0.033 ) and Bcl-2 ( F =115.916,P =0.001 ) when compared with the group of treatment astrocytes with H2O2.Conclusion These findings suggest that the attenuation of PTEN expression mediated by estrogen is associated with an increase in phosphorylation/activation of the Akt and the Bel-2 expressions.These results suggest that the protective effects of 17-β estradiol on the experimental model of SCI rats may depend on the estrogen protection to the astrocytes which may be mediated by decreasing the PTEN expression.