| Cerebrovascular disease is the cerebral dysfunction caused by the cerebral vascular pathological changes. Along with the elevation of standard of living and aging of the global population , cerebrovascular disease,heart disease and malignancy are the three deadly pathogeny in human being, therefore,the rate of incidence , disability ,mortality and relapse rate of cerebrovascular disease are high altogether . In recent year, the epidemiologic data indicates that the rate of incidence and mortality of cerebrovascular disease is higher than that of heart disease, at the same time,the incidence age is former and the popular age is later.Cerebrovascular disease not only affect the health of sufferer, but also affect the quality of living and subsistence, which bring heavy mental and economic burden to the family and society . The credibility and stability of experimental result is directly affected by the ideal animal model which is close to cerebral ischemia . So, controlling the danger factor of cerebrovascular disease and choosing the reasonable way to cure it can slow the course of disease and reduce the rate of incidence and mortality. Neurotrophins is an important sort of cerebrovascular disease, which can prevent neuron death and apoptosis of cortex and hippocampus from excitatory toxicity and peroxidation , but its molecular weight is high and can not get across the blood-brain barrier, so its clinical application is limited. Studying the proper administration is the better foreground toneurotrophins , which can provide new pathway and method to cure cerebrovascular disease.bFGF is discovered by Gospodarowicz from the cerebrum and pituitary of cow which physical and chemical method is applied, bFGF is the basic polypeptide which is composed of 155 amino acids and its pH is 9.6. It is sensitve to heat and acid , which is easily degraded by protease , it is generally distributed in cerebrum, heart, liver, bone, suprarenal gland and placenta, which is abundant in nerve tissues, especially in cerebrum and pituitary. The content of bFGF in cerebrum from high content to low is hippocampus, cerebral hemisphere,olfactory bulb,basal forebrain,cerebellum and exsists in cytoplasm and nucleus of astrocyte,and high molecular weight in nucleus ,low molecular weight in cytoplasm. The biological effect of bFGF is widespread, it can retain cell shape and migration function, facilitate cell differentiation and proliferation ,defer cell aging, reverse the aging cell , nourish neurons, gliocyte and vascular endotheliocyte directly , at the same time ,it can dilat cerebral vessels ,resist nervous toxicity from NO and SOD , stabilize Ca2+ channel and prevent the death of neurons.The aged Wistar rats of the experiment is carried on the reformed Pulsinelli-Brierley 4 blood vessels occlusion to make the animal modle of global cerebral ischemia/reperfusion. We observe cellular morphologic changes by HE dyeing , and test the dynamic expression of bFGF indifferent cerebral zone through immunohistochemistrical method , so we can analyze the protective effect on cerebral ischemic/reperfusion injury in different time .The results are in follows:1. HE dyeingThe control group: The morphology of nervous cells is normal , the structure is entire , the arrange of cells is tidy and clear , the boundary is clear ,the cytoplasm is light pink and the nucleus is blue , the outline of nucleus is clear which presents oval or round ,there is no necrotic cell and no edema.After cerebral ischemia/reperfusion , nervous cells express different degree of shrinkage,degeneration or necrosis,and also exists gliocyte proliferated.2. The dynamic expression of bFGF in different cerebral zone in rats . In control group, bFGF is expressed all in hippocampus, frontal lobe ,cerebellum and thalamus,cytoplasm or nucleus is dyed brown,the cells present round,oval or triangle.In hippocampus,bFGF begins to express at reperfusion 1h, and reach its expression peak at reperfusion 4d, at reperfusion 9d it gets back to the normal level.In frontal lobe,the expression of bFGF begins to increase at reperfusion 1h,and the expression peak is at 2d,at 9d, bFGF becomes normal. In thalamus ,the expression of bFGF present abruptly increasing fromreperfusion 2d to 4d,then begins to fall, and at 9d becomes normal level.In the molecular cell layer ,the Purkinje cell and medulla layer of the cerebellum,bFGF expresses at ischemia/reperfusion 1h ,and reaches a peak at 2d ,then from reperfusion 4d-9d , bFGF begins to decline but it does not yet returne to the normal levels ; In the cerebellar granular cells , the expression of bFGF in different reperfusion time has no significant difference comparing with the control group.At normal condition ,there is light expression of bFGF in cerebrum , and the expression is significantly increased . The protective mechanism of bFGF to ischemic neurons as follows : 1. To prevent neurons from apoptosis;2. To repair injured neurons; 3. To resist toxicity from excitatory amino acid,and maintain stability of calcium ion;4. To enhance the activity of antioxidyze and inhibite the expression of nitricoxide synthase to prevent injury from free radium; 5. To prevent nervous toxicity from NMDA.So,in the process of ischemic injury,not only the hypoxia and failure of energy ,but also the series of electrochemistrical reaction are the important mechamisms on ischemic injury.We can draw the following conclusions from the experiment :There is some extent expression of bFGF in the cerebrum of rats.Hippocamus is sensitive to ischemia /reperfusion , and the protective effect lasts longer in hippocampus; The frontal lobe is also sensitive to ischemia, but the protective effect of bFGF presents earlier and lastsshorter; Thalamus is not sensitive to ischemia,the protective effect of bFGF presents later and lasts shorter. Apart from cerebellar granular cells, other parts of the cerebellum sustain lasting protective mechamism for cerebral ischemia/reperfusion, but the cerebellar granular layer is not sensitive to ischemia.
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