Objective    To explore the effect of 17β-estradiol on rat cortical neurons injured by oxygenglucose deprivation (OGD).     Methods    Primary cortical neurons were isolated from neonatal rats and identified with NSE staining

then cultured for 10 d under normal condition. To establish OGD injury

the culture medium was replaced by glucose-free medium

and cells were transferred to a humidified incubation chamber flushed by a gas mixture of 95% N

2

and 5% CO

2

at 37 ℃ for 2 h. To explore the influence of 17β-estradiol on neurons under OGD for 2 h condition

the cells were pretreated with 10

-8

mol/L 17β-estr

adiol 24 h prior to OGD. The cell viability were evaluated by 3-(4

5-Dimethylthiazol-2-yl)-2

5-diphenyltetrazolium bromide (MTT) assay

and the percentage of apoptotic cells was tested by flow cytometry and Hoechst 33342 staining. The contents of MDA and the activities of SOD were evaluated by biochemical methods.     Results    The results showed that OGD injury significantly decreased the cell viability and the activities of SOD

increased the percentage of apoptotic cells and the content of MDA (P0.05). Pretreament of 10

-8

mol/L 17β-estradiol increased the cell viability and the activities of SOD

decreased the contents of MDA and the percentage of apoptotic cells in cortical neurons exposure to OGD (P0.01).     Conclusion    17β-estradiol has the neuroprotective effect on cortical neurons after OGD injury. This effect of 17β-estradiol may be mediated by eliminating the free radicals by increasing the activities of antioxidative enzymes and thus inhibit the oxidative damages caused by OGD.