| ObjectiveIn this study,we established rat VD model after chronic cerebral ischemia by modifiedligating bilateral common carotid artery.In order to to study the effect of eugenoltreatment on learning and memory impairment caused by VD through olfactorypathway.On the other hand, in order to test the changes of Glutamate energic neuronsin the hippocampus of VD rats after treated by eugenol using immunohistochemistrymethods. Primarily to study the effect and mechanism of eugenol treated onlearning and memory impairment caused by VD through olfactory pathway.Methods1.Preparing VD rat model. A modified2VO approach, namely as the right commoncarotid occlusion with a week later ligated the left one to estabilish VD model.2.Themechanism and efficacy of VD rats treated by eugenol.45adult male Sprague-Dawleyrats were randomly divided into3groups：(1) VD group(n=18). The rats in thisgroup submitted to the right commonn carotid occlusion with a week later ligated theleft one.7days,30days and60days after the surgery,the learning and memorycapacity was tested by Morris water maze.In this test,the escaping latency of the ratsto find the hidden platform in orientation navigate test and the numbers of rats crossingthe former platform in spatial probe test were recorded.The time was limited within120seconds. After the behaviours test,the rats were decapitated. Brains were putout and made into paraffin sections. After that we observed the pathohistologystructure of specimen by HE dyeing and sized up the Glutamate energic neurons inthe hippocampus by Glu-Ab.(2)Treatment group(n=17).The rats in this group received the same surgical procedures as the VD group.Besides that,this group were treatedwith eugenol(the consistence is1%)3days after surgery twice a day， and each timelasted30minutes.Then the rats in this group get the same procedures as the VDgroup.(3) Normal control group(n=10),the rats were not gave surgery and treated witheugenol.Then the rats in this group also got the same procedures as the VD group.Result1.7days after surgery， in Morris water maze test. The escaping latency and thenumbers of rats crossing the former platform had no significant differences in thelearning and memory capacity between each group (P>0.05).2.30days after surgery，there was significant differences between treatment group and VD group in the latencyand the times through platform(P<0.05). Aslo compare to normal control group，VDgroup had significant differences in the latency and the times through platform(P<0.05).3.60days after surgery， there was significant differences betweentreatment group and VD group in the latency and the times through the formerplatform (P<0.01). Aslo compare to normal control group， VD group hadsignificant differences in the latency and the numbers through the former platform(P<0.01).4.Compare the two estimation indices of7days to that of30days and60days of the VD group and the treatment group.there was significant differencesbetween them in both VD model group and the treatment group（P<0.05）.5..In theresults of immunohistochemistry,compare to normal control group,Glutamate energicneurons in the hippocampus of VD group rats were significantly decreased (P<0.01).Also the Glutamate energic neurons in the hippocampus between the treatment groupand VD group rats were significantly different(P<0.01).Conclusion1. The VD rat model produced by the modified ligating bilateral common carotid artery had less traumatic brain injury，but with significant learning and memoryimpairment. This is fitting with the clinical features of VD.2.In the60days aftercerebral ischemia,with the prolongation of the duration of ischemia,learning andmemory impairment was more serious.3.After the treatment of eugenol, the learningand memory impairment was improved.So eugenol can improve learning and memoryimpariment of vascular dementia through olfactory pathway.4.The mechanism ofeugenol improving learning and memory impariment of VD rats was related to theinhibition of decline of the Glutamate energic neurons. |
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