Objective:To investigate the protective effective of Rehmannia glutinosa oligosaccharides (ROS) on neural apoptosis and expression of apoptosis-related proteins in hippocampus CA1 region of vascular dementia rats. Method: SD rats were randomly and evenly divided into sham-operation group

model group

high and low dose of ROS treated groups. Vascular dementia model was established by repetitively blocking bilateral common carotid arteries and refilling. Behavioral score was used to evaluate the behavioral disorders of rats. HE staining was used to observe the pathological morphological changes in the neural cells of hippocampus CA1 region. The apoptosis of nerve cells in hippocampus CA1 region were detected with TUNEL method. The expression of B cell lymphoma/leukmia-2(Bcl-2) and Bcl-2 assaciated x protein (Bax) protein in the neural cells of hippocampus CA1 region were detected by immunohistochemical staining. The contents of glutamic acid in hippocampal tissue were detected by spectrophotometry

and superoxide dismutase(SOD) activity and malondialdehyde(MDA) contents in hippocampal tissue and serum were detected by the same method. Result: ROS could significantly reverse the ischemia-reperfusion induced increasing in behavioral score. It prevented the pathological morphological changes in hippocampus CA1 region. And it decreased the percentage of apoptotic cells in this area. Through ROS treated

the expression of Bcl-2 protein was significantly increased

while the Bax protein was decreased in this area. The Bcl-2/Bax was increasing. In addition

ROS could slow down the accumulation of MDA. It increased the activity of SOD in the serum and hippocampal tissue

while the production of glutamic acid decreased. Conclusion: ROS significantly alleviated the apoptosis of neuron in hippocampus CA1 region of vascular dementia rats

which was associated with influencing the expression of apoptotic proteins. In addition

the reducing of glutamic acid and MDA content

and the increasing of SOD activity indicated that ROS had protected effect to vascular dementia rats.