| Objective: Ischemic cerebral vascular disease (ICVD) is the common disease with morbidity and disability.It seriously threatens the health of the being,affects the living quality of the patients and their families,and draws more and more attention. Brain-derived neurotrophic factor(BDNF) and synaptophysin(SYN) play an important part in neural growth ,regeneration,reparation and synaptic plasticity after cerebral ischemia. However, there are different opinions about the expression of BDNF and synaptophysin.Sodium cytidine triphosphate(CTP)is a kind of nucleic acid,it has a lot of actions,it can stabilizes the cellular membrane, protects the enzyme activity,supports the cellular living and improves damaged neural regeneration and reparation.　Recently,it was used to treat anoxic ischemic encephalopathy, but the effect on histopathology and regulation of the synapse of it was reported rarely.In this experiment, a middle cerebral artery occluding rat model was made to investigate the pathological changes and the expression of synaptophysin and brain-derived neurotrophic factor and the regulatory effect of sodium cytidine triphosphate with HE staining and immunohistochemistry staining technique. The purpose of this experiment is to explore the relationship between the cerebral ischemia insult and the expression of SYNand BDNF, and the regulation of CTP on the synapticplasticity and the protection of the neural injury, and the mechanisms of CTP. By this study, we could establish a theory to study the synaptic plasticity after cerebral ischemia and treat cerebral ischemia.Materials and methods: Experiments were performed on healthy SD adult rats, males(33) and females(33) ,weighing 280～300g,offered by the animal center of HeBei Medical University. Referenced the reported method by Zea longa, Cerebral ischemia was induced by permanently occluding the distal middle cerebral artery. The rats with typical symptom were randomly divided into operated group and CTP-injected group (n=20),and sham-operated group (n=20) matched control. CTP (70mg/kg IP saline) was given to rats just after the end ischemia once a day until killed, and saline was given to rats in sham- operated group and operated group. After 7,14,21 and 30 days of ischemia.The rats were anesthetized with 1% pentobarbital sodium , fixed with 4% polyformaldehyde and killed. Removed the cerebral parietal cortex (between optic chiasina and marnmillary body). Embedded with paraffin and sectioned as usual. Stained with HE and immunohistochemistry to observe the morphology of ischemic neurons and the expression of SYN and BDNF in the hippocampal subfields CA3.The optical density of SYN and BDNF were measured by the picture analysis system.Results: 1.HE staining:In sham-operated group, the neurons in cerebral parietal cortex were distributed in 6 layers(ie, molecular layer, external granular layer, external pyramidal layer, internal granular layer, internal pyramidal layer and polymorphic layer).The neurons were dense and lined tidily. Cells were in normal shape and thenumber was numerous. Nucleus were large, spherical and purple. Cytoplasm was pink. In operated group after 7 days of ischemia, the degenerated and necrotic areas were seen in the parietal cortex, where the neurons of the pathological changes were slight. The neurons lined disorderly and turned into triangular or irregular, the soma slightly swollen, cytoplasm were ocidophily,and nucleus were pyknotic and intensive staining. Some neurons were also seen wrinkle, around which were blank areas. After 14 days of ischemia, the degenerated and necrotic neurons increased in number. A pile of neurons were loss, nucleus were more pyknotic compared with that of after 7 days of ischemia. After 21 and 30 days of ischemia, the number of degenerated and necrotic neurons were numerous, the area of infarction expanded, the pyknosis and vacuolar degeneration of the nucleus were observed in cell bodies. In the hippocampal subfields CA3, the degenerated neurons were observed after ischemia for e... |
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