| Objective:Establish a rat model of acute cerebral ischemia/reperfusion. Observe the ischemic and necrosis of the rats'brain and discuss about the possible mechanism of microthrombosis. Investigate the expression of fgl2 in the brain of this model and discuss the relationship between the expression of fgl2 and brain microthrombosis.Method:Part I. 72 male SD rats randomly divided into sham-operated control group (N=36), cerebral ischemia/reperfusion group (N=36). Each group randomly divided into 1 day group (N=12), 3 days group (N=12), 7 days group (N=12) by the reperfusion time. TTC staining was used to observe the infarction areas. HE and mason staining were used to detect the microthrombosis in rats'brain.Part II. Detect the expression of fgl2 in cerebral by immunohisto-chemistry method. Detect the expression of fgl2 in cerebral by western blot.Results:Part I 1. TTC staining showed no-reflew and necrosis in cerebral ischemia/reperfusion tissues. 2. HE staining showed disordered ranged cells in cerebral ischemia/reperfusion tissues. 3. Mason staining showed in situ thrombosis in microvascular of model group, and there was no thrombosis of sham group.Part II 1. Immunohistochemistry showed expression of fgl2 in microvasculature. 2. Western blot showed expression of fgl2 in brain increased in cerebral ischemia/reperfusion rats.Conclusion:There is microthrombosis in situ of cerebral ischemia/reperfusion rat model. The brain has microcirculation dysfunction in this model, which leading to hypoxia and necrosis. Increased expression of fgl2 in cerebral microvascular endothelial takes part in situ thrombosis. |
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