ABSTRACT
Objective To modify a classic two-vessel occlusion (2VO) modeling method in order to decrease the systematic errors in the behavioral experiments such as Morris water maze.Methods Thirty-two adult male Wistar rats were randomly allocated into classic 2VO model,modified model,sham operation and sham ligation groups (n =8 in each group).Only the bilateral common carotid arteries were ligated in the classic 2VO model group; the common carotid arteries were clipped intermittently,and the origins of pterygopalatine arteries of the internal carotid arteries were high selectively ligated in the modified model group; the common carotid arteries were only ligated intermittently in the sham ligation group; and only the common carotid arteries and the upper segment of pterygopalatine artery branches were separated in the sham operation group.The rat behavior was evaluated using the pupillary light reflex,Morris water maze and eight-arm radial maze.HE staining was used to observe the histological changes.Results The Morris water maze escape latency (F =72.169 - 163.102,all P ＜ 0.001) and the number of reference memory errors of eight-arm radial maze (F =33.515-74.726,all P ＜0.001) in the modified model and the classic 2VO model groups were longer and higher than those in the sham operation group.The pupillary light reflex of the rats was lost in the classic 2VO model group and the pupillary light reflex of the rats was normal in other groups.The reaching platform time in the classic 2VO model group was significantly longer than that in the modified model and sham operation groups (P ＜0.001).The percentage of target quadrant dwell time was also decreased significantly (at day 7 after procedure:F =13.770,P ＜0.001 ; at day 90 after procedure:F =14.780,P ＜0.001).HE staining showed pathological changes such as the cells decrease in hippocampal CA1 region and leukoaraiosis in the modified model and the classic 2VO model groups.In addition,there were more vacuole-like changes in the rat optic nerve region in the classic 2VO model group,while there were no such changes in the modified model group.Conclusions Establishing vascular dementia model with permanent occlusion of bilateral internal carotid arteries after intermittent occlusion of bilateral carotid arteries could avoid severe visual impairment in rats.In the Morris water maze and eight-arm maze test,the modified model rats showed significant decrease in learning and memory abilities and had hippocampal damage.
ABSTRACT
Objective To investigate the effect of U0126 on brain edema and the expression of aquaporin 4 (AQP4) in rat brains after cerebral ischemic injury.Methods Totally 48 healthy male SD rats were divided randomly into ischemia group, treatment group and normal group.Rats in ischemia group and treatment group underwent middle cerebral artery occlusion by using an intraluminal thread method.Thirty minutes before operation, the rats in treatment group were injected into lateral cerebral ventricle with U0126, while rats in ischemia group accepted normal saline.24 hours after operation, the water content and Evans Blue in rat brains were determined as to exploring the degree of brain edema.Immunohistochemistry,Western blot and RT-PCR technique were applied to detect AQP4, p-ERK1/2 and p-ELK1.Results Compared with normal group, the water content and AQP4 expression in ischemia group were increased obviously.The water content and AQP4 expression in treatment group (protein:149.0?1.1,mRNA:0.328?0.010) were lower than those in ischemia group (protein:153.6?0.8,mRNA:0.400?0.015,P
ABSTRACT
Objective To elucidate the delayed neuron death and the expression of ?-amyloid protein (A?) in hippocampus after reperfusion of transiently ischemic lesion.Methods Immunohistochemical and HE technique was used to examine the delayed neuron death and expression of ?-amyloid protein at 6 h,2 d,3 d,7 d,14 d,35 d after reperfusion of transiently incomplete forebrain ischemia in rat hippocampus.Results Delayed neuron death was seen at 3 days after ischemia/reperfusin in CA 1 area of the hippocampus. A? immunoreactivity began enhanced at 2 d (A:0.082?0.011)after reperfusion, up to peak at 7 d(A:0.175?0.024), disapeared at 35 d.Conclusion Delayed neuron death was occurred after reperfusion of transiently incomplete forebrain ischemia in rat hippocampus,and at the same time, A? was up expression, which is suggested to be an important role of A? in neuron death after reperfusion of ischemic lesion.