Objective To investigate the effects of resveratrol （RSV） on the cognitive function of rats with vascular dementia （VD） and on the silent information regulator 1 （SIRT1）/forkhead-box transcription factor O3a （FoxO3a） pathway.Methods Forty clean-grade healthy male Sprague-Dawley rats were randomly divided into four groups： sham operation group， VD model group， low-dose RSV group （30 mg/kg）， and high-dose RSV group （60 mg/kg）， with 10 rats in each group. The VD rat model was established by bilateral common carotid artery occlusion. In the sham operation group， the bilateral common carotid arteries were isolated and suture was placed around the arteries without occlusion. Rats in the treatment groups were intragastrically administrated corresponding doses of RSV. The sham operation group and the VD model group were given an equal volume of sodium carboxymethyl cellulose solution. Morris water maze was used to test the spatial learning and memory ability of rats in each group. HE staining was used to observe the pathological changes of neurons in the hippocampal CA1 region of rats in each group. TUNEL staining was performed to observe the apoptosis of neurons in the hippocampus CA1 region of rats in each group. Western blotting was used to measure the expression of SIRT1， FoxO3a， B-cell lymphoma 2 （Bcl-2）， Bcl-2-associated X protein （Bax）， microtubule-associated protein 1 light chain 3 （LC3）， and Beclin1 in the hippocampus of rats.Results Compared with rats in the sham operation group， the VD model group showed significantly longer escape latency （P<0.05）， a significantly reduced percentage of residence time in the target quadrant （P<0.05）， more severe neuronal damage in the hippocampal CA1 region， a significantly increased number of apoptotic neurons （P<0.05）， significantly decreased expression of SIRT1， FoxO3a， Bcl-2， and Beclin1 （P<0.05）， significantly increased expression of Bax （P<0.05）， and significantly decreased ratios of Bcl-2/Bax and LC3 II/I （P<0.05）. Compared with rats in the VD model group， rats in the RSV treatment groups showed significantly shorter escape latency （P<0.05）， a significantly increased percentage of residence time in the target quadrant （P<0.05）， significantly reduced pathological damage of hippocampal CA1 neurons， significantly decreased neuronal apoptosis （P<0.05）， significantly increased expression of SIRT1， FoxO3a， Bcl-2， and Beclin1 （P<0.05）， significantly decreased expression of Bax （P<0.05）， and significantly increased ratios of Bcl-2/Bax and LC3 II/I （P<0.05）. There were no significant differences between the high and low doses of RSV （P>0.05）.Conclusions RSV can improve the cognitive function of VD rats， reduce hippocampal neuronal apoptosis， activate autophagy， and exert neuroprotective effects. The mechanism may be related to activation of the SIRT1/FoxO3a pathway.