Objective      To explore the change of oxidation/antioxidation balance from 1 h to 21 d after bilateral common carotid artery occlusion (BCCAO) in hippocampal CA1 region

and further to reveal the molecular mechanism of neuron damage in the early stage of vascular dementia.       Methods      Adult male Sprague-Dawley rats were randomly assigned into 2 groups: sham group and BCCAO groups (1 h

and 1

3

7 and 21 d). The markers of oxidative stress damage and anti-oxidant level in hippocampal CA1 region were detected by laser scanning confocal microscopy (LSCM) and Western blot analysis. The neuron

vascular and astrocyte ultrastructures were observed after BCCAO in hippocampal CA1 region by transmission electron microscopy (TEM).       Results      Compared with the sham group

the fluorescence intensity of HEt (oxygen free radical probe) were significantly increased in time-dependent manner (in  1 h and 3

7 and 21 d after BCCAO). Double immunofluorescent staining and Western blot results indicated that levels of 3NT (peroxynitrite radical marker) and 4HNE (membrane lipid damage marker) were significantly increased in the BCCAO 7 d and 21 d groups than the sham group (P0.05). Compared with the sham group

the levels of antioxidant transcription factor Nrf2 and its downstream antioxidation products SOD2 and HO-1 were significantly decreased in the BCCAO 7 d and 21 d groups (P0.05). Ultrastructure analysis revealed that different degrees of damage were found in the neuron

vascular and astrocyte ultrastructures at 1 h

3 d and 21 d after BCCAO in hippocampal CA1 region. And the damage was the most serious in the BCCAO 21 d group

showing chromatin edge accumulation

dissolved nuclear membrane

swollen mitochondria

dilatation of endoplasmic reticulum

as well as severe edema around the blood vessels.       Conclusion      The damage of hippocampal CA1 neuron is increased in time-dependent manner at the early stage of vascular dementia

and the mechanism may be closely related with the intracellular oxidation/antioxidation imbalance after BCCAO.