| Background and objective:With the population aging in our country, the incidence of the dementia is increasing year by year. Vascular dementia (VD) and alzheimer’s disease (AD) accounted for most of dementia, and the incidence of VD is higher than AD. Dementia brought serious economic and mental burden for the whole society and his family. In recent years, both VD and AD have been considered with vascular factors. Chronic cerebral ischemia is a common pathological state of nervous system, which is caused by the long time insufficient of cerebral perfusion. This pathological state as a common pathological process of VD, Binswanger disease and AD, can lead to the disorder of cerebral metabolic and function. It’s more and more important to explore the mechanism of dementia which caused by the cerebral hypoperfusion. Many studies have been done for the cognitive impairment caused by chronic cerebral ischemia, such as:cerebral metabolism, cerebrovacular damage, the activity of immune cells, cell apotosis, synaptic structure and so on. Numb was firstly found in the development of the peripheral nervous system in drosophila. Numb can decide the cell fate in drosophila, that’s why it was called as cell fate determinant. Then the function of cell fate decision has also been found in mammals and people. The structure and function is more complex in mammals than in drosophila. Numb as an endocytosis protein plays an important role in the nerve development process in recent studies. Numb not only pateicipates in the adjustment of the asymmetric division of neural precursor cell, maintain the neural progenitor cells’s self-refreshment, but also participates in the regulation of nerve cell’s migration and the neurite growth. In order to investigate the relationship and its possible mechanism of the expression of Numb in the hippocampus and the congnitive function after chronic cerebral ischemic, we will detect the congnitive fuction and the expression of Numb in the hippocampus in aged chronic cerebral ischemic rats to provide the basis theory of the research and treatment for the cognitive impairment caused by ischemic cerebrovascular disease.Materials and methods:1.40healthy male SD rats(age more than12months) were divided into four groups at random:sham-operated group, experimental groups of8weeks,10weeks and12weeks.2. The chronic cerebral ischemia models were produced by permanent occlusion of bilateral common carotid arteries (2VO model), the sham-operated group accept the same operation except occlusion of bilateral common carotid arteries.3. The performance in Morris water maze of each group at the right time was investigated to explore the learning and memory ability of rats.4. The expression of Numb in the CA1of hippocampus was measured by immunohistochemical technique.5. The expression of Numb in the hippocampus was measured by Western blotting.6. Data collection and data analysis. Results1. As compared with the sham-operated rats, the experimental groups showed a significantly increased latency of the rats to find the hidden platform and the times of crossing the platform zone when the plateform was removed had a significantly diminished in Morris water maze task, this would be more obvious when the time of cerebral ischemia was longer. It was indicated that the spatial learning and memory abilities of2VO rats were sharply impaired and with the extension of ischemia time this situation would be more serious.2. As compared with the sham-operated rats, the expressions of Numb in the CA1of hippocampus of experimental groups which measured by immunohistochemical technique was notebly decreased, and with the extension of ischemia time the expressions of Numb would be less and less.3. As compared with the sham-operated rats, the expressions of Numb in the hippocampus of experimental groups which measured by Western blotting was notebly decreased, and the expressions of Numb would be less and less when the time of cerebral ischemia was longer.Conclusion:1. In the rats8-12weeks after2VO, as the extension of ischemia time, the cognitive function was damaged and the expression of Numb in the hippocampus was declined.2. The decline expression of Numb after chronic cerebral ischemia may play an important role in cognitive impairment of aged rats. |
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