The Time-variation Of β-amyloid Protein Deposit In Three Different Area After Local Cerebral Ischemia In Rats

IntroductionIschemic cerebrovascular diseases have threatened human health even life more and more seriously. Through several different pathological and biochemistrical mechanisms cerebral tissue is damaged by ischemia.β-amyloid protein(Aβ) is a 39-to 43-amino-acid peptide produced from amyloid precursor protein (APP). Aβ, major component of senile plaques in Alzheimer's disease, has been implicated in neuronal cell death. Cerebral ischemia leads to a upregulation and accumulation of Aβbut the mechanism underlying Aβneurotoxicity remains unclear.Methods1. Animals and groups: Animals were divided into three groups: normal control group (n=6), sham operation group (n=6) and test group (MCAO group, n=18). Rats in test group were subjected to 2-hour middle cerebral artery occlusion. Rats in sham operation group were performed the same procedures with test group except occlusion of middle cerebral artery.2. Immunohistological assessments: Immunohistological assessments were performed to examine the expression of Aβ. Taken two sections of each sample, examined and photographed using computerized video imaging microscopy.3. Statistical Analysis: All data were expressed as (?)±s. The results were analyzed using ANOVA and processed by SPSS 13.0. A value P＜0.05 was considered statistically significant.Results1.The time-variation of Aβdeposit in three different areas of ischemic hemisphere: There is no significant difference between sham operation group and normal control group in Aβdeposit (P＞0.05). Aβdeposit in test groups is significant higher than sham operation group and normal control group (P＜0.05) and gradually decreases (P＜0.05).2. Various time three cerebral areas Aβdeposit quantity comparison: Three cerebral areas Aβdeposit quantity are different at 1W and 4W (P＜0.05), the cerebral cortex Aβdeposit quantity is significant higher than hippocampus (P＜0.05), three cerebral areas Aβdeposit quantity are not difference at 2W (P＞0.05).Conclusions1. There is Aβdeposit in crerbral cortex, hippocampus and thalamus after cerebral ischemia in rats, the deposition of Aβgradually decreases.2. Aβdeposit in crerbral cortex is higher than hippocampus after cerebral ischemia.