| Cerebrovascular disease is a clinical disease and is one of the three lethal diseases. Clinical cerebral artery disease involves ischemic cerebrovascular disease and hemorrhagic disease, especially ischemic cerebralvascular disease is prevalent. There is great harm in ischemic cerebralvascular disease especially after cerebral ischemia-reperfusion injury.Cerebral ischemia-reperfusion injury is cerebral ischemia induced brain injury and ischemic injury has further aggravated their situation after restoring blood perfusion.Neuron injury induced ischemia-reperfusion(IR) is the result of many factors: ischemia-reperfusion injury(IRI) increases production of free radicals and a variety of neurotransmitters,excitaxory amino acid(NMDA receptor)together,which make Ca2+ channel open and intracellular calcium overload. Increased intracellular Ca2 + also accelerates the production of free radicals and the emergence of common caused reperfusion injury. The blood-brain barrier destruction is the important phthophysiological basis of IRI.Neuronal death after ischemia displays necrosis and apoptosis of the two main forms, relating to active and passive cell death mechanisms. Cerebral ischemia in the acute phase, neuronal necrosis and apoptosisare concomitant. Necrosis is in the center of ischemic areas, and apoptosis occurred mainly in the ischemic penumbra; and the delayed neuronal death in brain ischemia period allocated mainly apoptosis. Apoptosis may decide the final infarct volume. Thus inhibition of apoptosis, saving ischemic penumbra,to reduce IRI is of great significance.IGF-1 is discovered by Salmon and Danghaday in the early sixties of the twentieth century. Under physiological conditions, the central nervous system has a broad IGF-1 in immune response and IGF-1mRNA expression. The highest content is in pituitary, the second is the olfactory bulb and upper brainstem, cerebellum is followed, striatum, hippocampus, lower brain stem and cerebral cortex. IGF-1 is an important bioactive substance as a mean of regulating nerve growth in a variety of pathological conditions after IR, IGF-1 plays an neurotrophic protective effect by inhibiting the neuronal apoptosis.Choosing aged Wistar rats and adopting the modified method of Pulsinelli-Brierley 4 vascular occlusion make the animal model of whole cerebral ischemia-reperfusion in this experiment. Observe morphologic changes of the brain tissue by HE staining. Detecting the dynamic expression of IGF-1 in different brain regions at different times after cerebral IR in rats by using immunohistochemical staining method,further exploring the neurotrophic protective effect of IGF-1 on IRI. The results are as follows:1. HE staining:Control group: normal morphology, tight cells, neat, uniform distribu -tion, membrane integrity, light pink cytoplasm, blue nuclei, and clear nucleolus.Experimental group: varying degrees shrinkage, nuclear condens -ation, cell necrosis, glial cells can be seen.2. The expression of IGF-1 in the central nervous system of the rats after cerebral IR.There is a certain level of IGF-1 expression in cerebellum,hypothalamus,hippocampus and the frontal lobe in normal aged Wistar rats.In the cerebellum: the expression of IGF-1 increases slightly at 1h after IR in the molecular layer, but no significant difference compared with the control group. IGF-1 expression is significantly increased at 6h after IR and reaches a peak on 2d after IR. On the 4th day of reperfusion the expression of IGF-1 drops to a basis level and increases on 9d after reperfusion; In Prukinje layers, IGF-1 expression increases slightly at 1h after IR, but no significant difference compared with the control group. IGF-1 expression is significantly increased at 6h afterIR,and reaches a peak on 2d after IR. IGF-1 expression decreases slightly on 4d after IR, but no significant difference compared with the control group. IGF-1 expression is increasing in turn on 9d after IR; In Granule cell layer, IGF-1 expresses less and has smaller changes after IF,and has no significant difference compared with the control group; In medulla layer, the expression of IGF-1 increases slightly at 1h after IR, but no significant difference compared with the control group. IGF-1 expression is increased significantly at 6h after IR, and reaches a peak on 2d after IR. The expression of IGF-1 drops back to basis on 4d after IR, and IGF-1 expression futher increases on 9d after IR.In the hypothalamus, the expression of IGF-1 increases at 1h after IR, and increases significantly at 6h after IR, and IGF-1 expression reaches a peak on 2d after IR, then rapidly decreases on 4d after IR, and further reduces on 9d after IR.In the hippocampus, the expression of IGF-1 increases slightly at 1h after IR, but no significant difference compared with the control group. IGF-1 expression is significantly increased at 6h after IR, and reaches a peak on 2d after IR, then the expression of IGF-1 begins to decrease and is significantly less than the control group on 4d after IR, IGf-1 expression further reduces on9d after IR.In the frontal lobe, the expression of IGF-1 increases slightly from 1hto 6h after IR, but no significant difference compared with the control group, IGF-1 expression has a transient increase on 2d after IR, then the expression of IGF-1 rapidly decreases and drops back to the basis level on 4d after IR, and further reduces on 9d after IR. Conclusions: Adopting the modified method of Pulsinelli-Brierley 4 vascular occlusion can make the whole animal model of cerebral ischemia-reperfusion.There is a small amount of IGF-1 expression in normal brain tissue. In cerebellar granule cell layer IGF-1 lacks neuronal protection, other cell layers IGF-1 has rapid and delayed neuronal protection. In the hypothalamus the neuronal protection of IGF-1 appears earlier, but reduces in the later part of IR. The neuronal protection of IGF-1 in hippocampal appears earlier, but in the later part of IR hippocampal lacks the protective effect of IGF-1 on neurons. IGF-1 in the frontal lobe has a quick and transient protection after IR. |
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