Mechanism Of Micro-Vascular Endothelial Injury And Apoptosis In The Rabbit Model Of Cerebral Ischemia

Objective: pathological change of cerebral ischemia is change of permeability and integrality of micro-vessel due to injury, resulting in neuron injury and a series of complication. The integrality of vascular due to vascular endothelial, including integrality of anatomy and barrier function, viz blood brain barrier and basement membrane. The endothelial of micro-vessel is the consructure basement, consisting of three layer master: cerebral vascular endothelial, basement membrane and the end feet of astrocytes. Laminin, component of the basement membrane, due to the vascular integrality and the degree of basement membrane injury. Cerebral infarction is related to the apoptosis of neuron cells, and the expression of Bax (Bcl-2 associated X protein). To observe the level of plasm Laminin with cerebral infarction and the expression of Laminin and Bax in the brain tissue in the model of cerebral infarction, we made cerebral infarction model in rabbit treated with defibrinogenase and to discuss its possible protective mechanism. The change of Laminin and Bax in the condition of hyperglycemia and hyperlipemia was observed simultaneously.Methods: 24 New Zealand rabbits were randomly divided into threegroups: normal control group, model control group, and defibrinogenase treated group. They were fed with high fat and high sucrose except the normal control group. We made the model of cerebral infarction with enjecting tiny emboli of themselves through right common carotid artery of rabbit. Then we treated them with defibrinogenase in the concerned group and normal saline in the control group. It was observed that the changes of blood lipids and blood glucose. The plasm concentration of Laminin was observed with the method of ELISA. All group received pathological examination and the section was stained with haematoxylin - eosin (HE). The expression of Laminin and Bax in brain tissue with ischemia was observed with the immuno-histochemical method of SABC (StreptAvidin-Biotin Complex), tested by integrated optical density (IOD) and positive proportion.Result: The level of blood lipids and blood glucose of rabbit had prominence increased after fed with high fat and high sucrose about one to two times in 10 days. Blood lipids and blood glucose had no prominence change after treated with defibrinogenase (P>0. 05) . The plasm concentration of Laminin was decreased prominently after the operation of cerebral infarction(P<0. 05). The plasm concentration of Laminin and the expression of Laminin in brain tissue significantly increased in the dedibrinogenase treated group compared with model control group(P< 0.05).In pathological observation, the edema of brain was alleviated in the defibrinogenase treated group compared with other two groups.The expression level of Laminin measured by integrated optical density was significantly increased in the difibrinogenase treated group compared with model control group (P<0. 05). The expression of Bax in cerebral tissue measured by integrated optical density were significantly decreased in the defibrinogenase treated group compared with modelcontrol group (P<0. 05) . The expression of Bax in cerebral tissue were significantly increased in the model control group compared with nomal control group (P<0. 05) .Conlusions: Injury of the micro-vessel endothelial exists in the early phase of rabbit cerebral ischemia model, leading to injury of micro-vessel and decrease of Laminin in extracellar matrix. Cerebral infarction is related to the apoptosis of neuron cells, and the expression of Bax (Bcl-2 associated X protein). Hyperglycemia and hyperlipemia can increase the expression of Bax in cerebral infarction. This study was confirmed to supply the experimental basis for defibrase applying to cerebral ischemia patients.