Changes Of The Active Of COX And The Ultrastructure Of Hippocampal Neurons Mitochondrion In Rats With Memory Deficit Induced By β-Amyloid Protein Fragmant25-35

Objective To study the relationship between the changes of the expression of COX and the ultrastructure of neuronal mitochondrion in the hippocampus CA1 of the animal model of AD induced by β-Amyloid peptide fragment 25-35, and to explore the neurotoxic mechanism of Ap.Methods 45 SD rats were choose and divided into three groups randomly: Aβ group, normal saline group and Sham operation group with 15 rats in each group. Aβ_25-35 2μl (5μg/μl) was stereotaxically injected into the right hippocampus CA1 in experimental group and the equal amount of normal saline was infused into the same area in control group. Y-shape maze task was conducted to check learning and memory activities before and 7 days after the injection of Aβ_25-35 or normal saline, respectively. With the method of enzyme histochemical staining, the activity of COX in rats' hippocampus CA1 were mensurated .8 days after the injection 3 rats were randomly taken from each group and the hippocampus CA1 in rats were dissected. The ultrastructural changes of neuron mitochondrion in hippocampus CA1 were viewed under transmission electron microscopeResults 8 days after injection of Aβ_25-35,the learning and memory ability of Aβ-injected rats were lower(P<0.05), and the number and modality of hippocampus neuron mitochondrion had distinct changes when compared with that of the controls. Furthermore, the activity of COX in hippocampus CA1 has decreased markedly in the animals model of AD than in the controls(P<0.05).Conclusion The role of Aβ in the process of neurodegeneration may be related to the failure of energy metabolism secondary to the inhibition of the expression of COX and the ultrastructural changes of neuronal mitochondrion.