Objective To observe the expression of autophagy and microtubule-associated protein 1 light chain 3 (LC3) in hippocampus CA1 area of vascular dementia rats, so as to explore the role of autophagy in the pathogenesis of vascular dementia. Methods The rats were randomly divided into sham operation group, vascular dementia model group (VD group) and Wortmannin autophagy inhibitor group (WM group). Each group was further divided into 1, 2, 4, 8 and 12 week subgroups after the successful model preparation (n=6). Vascular dementia rat models were established by blocking four vessels. The learning and memory abilities were examined by Morris water maze, autophagy was observed by transmission electron microscope, and the ratio of autophagy-associated protein LC3Ⅱ/LC3Ⅰ was obtained by Western blotting analysis. Results Compared with the sham operation group, the escape latency was signficantly increased in the VD group（P<0.05 or P<0.01）, and the times of traversing terrace were significantly decreased (P<0.05 or P<0.01). Compared with the VD group, the escape latency was significantly decreased and the times of traversing terrace was significantly increased in WM group (P<0.05 or P<0.01). In the hippocampus CA1 area of VD group, the nuclear membrane of neurons was sagged, the nuclei was condensed, mitochondria were swollen, and autophagosomes and lysosomes were observed in week 1; the autophagosomes and lysosomes were increased in week 4, and they could still be found in week 12. The neuronal damage was slighter and the autophagosomes were reduced in WM group compared with VD group. In CA1 area of hippocampus of VD group, the LC3Ⅱ/LC3Ⅰ ratio was increased in week 1, peaked in week 4, began to decline in week 8, and still kept at a high level in week 12. Compared with the VD group, the LC3Ⅱ/LC3Ⅰ ratio was significantly decreased in WM group at all time points (P<0.05 or P<0.01).Conclusion Autophagy is activated in CA1 area of hippocampus of VD rats, and may play an important role in the pathogenesis of VD.