| Objective:(1)Chronic cerebral white matter lesions is caused by a variety of reasons to lead to the long-term cerebral hypoperfusion, prompting the organization of brain occur pathology and biochemical changes. It has been proved to be a common pathological process, such as cerebral arteriosclerosis, vascular dementia, Alzheimer disease and Binswanger disease and other diseases. Present study suggests that white matter lesions (WML) are mostly the result of chronic ischemia.Previous studies have great importance to acute ischemic pathology and molecular biological changes in rats. In my study the main research that the chronic ischemic rat brain neurovascular unit pathologic changes after from 1 month to 3 month. White matter lesions can destroy neurons, destroy the cortex and subcortical signal transmission between the central, leading to cognitive impairment and gait abnormalities, Finally leading to persistent or progressive cognitive and neurological dysfunction. Study was designed to observe the brain neurovascular unit of pathological regular changes after chronic ischemic. In order to explore the early cerebral ischemia using VEGF and GFAP on the neurovascular unit to produce a protective effect.Method:Sixty Wister rats were randomly divided into sham operation group(thirty) and ischemia group(thirty), the experiment group was further divided into reperfusion for 3d,7 d,14d,1 month,3 months 5 subgroups. As far as survival 1 month to more than 3 months after ischemia. Each time taking five perfusion the brain, HE staining were used to examine the pathological changes in rat brain, immunohistochemical to examine the antigens of glial fibrillary acidic protein (GFAP), vascular endothelial growth factor (VEGF) and laminin were observed astrocytes,vascular endothelial cells and basallayer changes. Immunohistochemical detection of GFAP, VEGF, Laminin change after the 400 optical microscope, the count of five vision-positive cells, or capillary number. A single-factor variance analysis method, using SPSS13.0 were statistically analyzed, P<0.05 are statistically significant.Result:(1)sham-operated group the most of cell morphology are normal, occasional neurons degeneration and death. After three days ischemia can be seen hippocampus and cortex perivascular and interstitial edema,neuron shrinkage, cell swelling,interstitial and perivascular edema has been reduced,neuronal necrosis began to appear, astrocytes and capillary hyperplasia, with the extension of ischemic time, interstitial and perivascular edema disappeared, angiogenesis significantly, the number of normal neurons reducing and disordered, cells with irregular shape, uneven vacuoles within the cytoplasm. (2) Compare with the sham-operated group, ischemia 3d,7d,14d,1 month,3 months of increased GFAP expression, and astrocytes in general and the differences between groups were statistically significant (P<0.05). prompt reactive astrocytes hyperplysia after ischemia, ischemia 3 months GFAP can be seen scar tissue.VEGF expression in ischemic 3d and began to increase in ischemic 7d,14d and the three groups continued to increase as compared with the control group the difference was statistically significant (P<0.05), this phenomenon is consistent with previous reports.Ischemia 1 month,3 months VEGF expression in a decrease in acute, but still increased than sham group.3d ischemia can occur Laminin reduction in ischemic 7d reduce the most obvious, ischemia 14d,1 month,3 months Laminin expression gradually increased. Ischemia in 1 month and 3 month when the Laminin expression was gradually increasing trend, suggesting that the extracellular matrix in chronic ischemia in the process of gradually thickened, Laminin accumulation plays a major role. Statistics show that ischemia 1 month, 3 months Laminin expression compared with the sham group were significantly different (P<0.05), At the early period Laminin ischemia rapidly decreased,at late period Laminin abnormal accumulation.Conclusion:(1)Confirmed bilateral carotid artery ligation in rats is also a chronic ischemia successful model of neurovascular unite damage (2) At early ischemic neurons and glial cells, while damaged, shrinkage, swelling, lately eosinophilic change and necrosis, with the extension of ischemic time, glial cell proliferation, accompanied by angiogenesis. (3) Chronic cerebral ischemia in different time neurons, GFAP, VEGF, Laminin regular changes,GFAP in early ischemia resulting solid skeleton and neurotrophic effects, in late proliferative hypertrophic scar formation have a negative impact, At ischemic entire process VEGF have played active role,in future treatment may play an important role, Laminin at early ischemia reduction, the late accumulation can exacerbate atherosclerosis. At the same time the interaction among each other adjust. (4) Neurovascular unit was a victim in the ischemic progress, the existence of chronic ischemic neurovascular unit has self-repair process. After cerebral ischemia is not only neuron protection, we should also strengthen the glial cells, endothelial cells and basement membrane of protection.
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