Protective effect of resveratrol on chronic cerebral hypoperfusion-induced cognitive impairment in rats / 中华老年医学杂志

ABSTRACT

Objective To observe the effect of resveratrol on cognitive impairment in rats after chronic cerebral hypoperfusion,and to explore the underlying antioxidant mechanism of resveratrol.Methods The chronic cerebral hypoperfusion model was induced by permanent occlusion of bilateral common carotid arteries (2VO) in rats.Healthy male Wistar rats were randomly divided into 3 groupssham-operated group,2VO group and 2VO+resveratrol group.Spatial learning and memory were assessed using the Morris water maze at 4 weeks after the occlusion.The levels of 4-Hydroxynonenal (4-HNE) and 8-Hydroxy-2′-deoxyguanosine (8-OHdG) in the cortex and hippocampal CA1 areas were detected using immunohistochemistry staining,for reflecting the lipid peroxidation and oxidative DNA damage.Results The escape latencies from the third day to the fifth day were longer in 2VO group than in sham-operated group[(42.1+5.4)s vs.(25.1±3.3)s,(36.4±4.4)s vs.(12.4±3.3) s,(30.4±4.0)s vs.(8.1±3.4)s,q=10.91、14.54 and 14.07,all P ＜0.01],while the time spent in the object square was shorter in 2VO group than in sham-operated group[(12.9+2.5)s vs.(18.9+2.2)s,q=6.47,P＜0.01].Compared with 2VO group,the escape latencies in 2VO+resveratrol group from the third day to the fifth day were shorter[(29.5+4.0)s,(25.6±4.3)s and (19.8±4.2)s,q=7.71,6.22 and 6.37,all P＜0.01],while the time spent in the object square was longer[(16.5±1.8)s,q=3.83,P＜0.05].Compared with the shamoperated group,the mean integral optical density (IOD) of 4-HNE and 8-OHdG in the cortex and hippocampus CA1 area were increased in 2VO group (265.1 + 9.0 vs.168.2 + 6.0,37.8 + 5.0 vs.24.0+4.0,q=31.89 and 7.48,both P＜0.01).And in the 2VO+resveratrol group,the mean IOD of 4-HNE and 8-OHdG in the cortex and 8-OHdG in hippocampus CA1 area were lower than in 2VO group (195.1±7.0,26.0±4.3,q=23.03 and 6.49,both P＜0.01).Conclusions Resveratrol can improve the cognitive impairment in rats after chronic cerebral hypoperfusion,which may be related to preventing oxidative damage.