The Relationship Between Changes Of Behavior, NO And Synaptophysin And Alzheimer-phathology Changes After Chronic Cerebral Hypoperfusion

OBJECTIVE: (1)To build a chronic cerebral hypoperfusion model by ligating the bilateral common carotid arteries in rats;(2)To study the relationship between Alzheimer's Disease(AD) and nitric oxide(NO) changes in blood serum at different time after cerebral ischemia,and to study the relationship between AD and synaptophysin at different time after cerebral ischemia;(3)To study the expression ofβ-amyloid peptide (Aβ) and phosphorylated Tau protein at different period of cerebral ischemia, furthermore, investigate the relationship between chronic cerebral hypoperfusion and AD.MATERIALS AND METHODS: Thirty-six male Wistar rats aged 4 months were used. Rats were divided to three groups randomly: the cerebral hypoperfusion for 12 weeks, 16 weeks and 20 weeks; Further, every group were divided to two groups randomly: the cerebral ischemia and same-age control. There were 6 rats in every group. The cerebral hypoperfusion model of rats was made by ligating bilateral common carotid arteries with silk. The same-age controls were received the same operation but without occlusion of the arteries. Learning and remembrance ability of rats was tested by Morris water maze experiment at the 12th weeks, 16th weeks and 20th weeks after they were operated. The bloods were collected to detect serum NO concentration in by nitrite spectra-luminosity chromatometry, and measure serumβ-amyloid peptide (Aβ) levels with the method of balanced saturated competition radioimmunoanalysis. The animals were killed at 20th weeks, and whole brains were removed for immunohistochemistical staining of in Aβ, phosphorylated Tau-protein and synaptophysin. The positive gray value was calculated by Image analysis system.RESULTS: The rats'time latency and distance latency of every group with cerebral ischemia in Morris water maze experiment prolonged significantly as comparing with the same age control groups (p<0.05). All groups of cerebral ischemia contrasting using ANOVA (LSD), and the result showed that the time latency and distance latency shorten significantly in 16 weeks, 20 weeks than 12 weeks, and there is no statistical difference between 20 weeks and 16 weeks. The results indicate that chronic cerebral ischemia can damage rats'intelligence lesion.The gray value of Aβand phosphorylated Tau-protein immunohistochemistrical positive staining in cerebral cortex and hippocampus of the cerebral hypoperfustion rats was lower than the controls (The lower, the more positive staining is). It showed that chronic cerebral hypoperfusion induced by ligating may result in increase of Aβand phosphorylated of Tau-protein expression in brain, and further showed that chronic cerebral hypoperfusion maybe...