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脑缺血损伤可引起血脑屏障破坏,溶栓治疗可以再通血流,保护脑组织免受损伤,但可使颅内出血增加。脑脉通已被证实对脑缺血损伤有保护作用。本实验拟对脑脉通联合溶栓对脑缺血大鼠血脑屏障的保护作用及其可能的作用机制进行探讨。将实验大鼠随机分组;运用自体血栓结合线栓阻塞大鼠大脑中动脉制备血栓栓塞性脑缺血动物模型;大鼠缺血后3h、6h、9h经导管由区域动脉进行溶栓;动脉给药后24h观察大鼠脑组织颅内出血率变化,用免疫组织化学法测定脑组织IgG、IV型胶原蛋白(CoLIV)、尿激酶型纤维蛋白酶原激活物(uPA)和uPA受体(uPAR)表达的变化。结果显示,模型组大鼠脑内出血率增高,其9h、6h组IgG水平增高、CoLIV降低,各组uPA和uPAR表达明显;溶栓组颅内出血率较模型组增高,各用药组9h的IgG降低、Co-LIV增强,uPA和uPAR表达减弱;各组9h较3h和6h的IgG表达增强,CoLIV减弱,uPA和uPAR表达显著;联合组的颅内出血率较溶栓组降低,其9h组的IgG分别较脑脉通组降低、CoLIV增强,uPA和uPAR表达减弱。上述结果提示,脑缺血可引起血脑屏障破坏,溶栓可增加颅内出血率,脑脉通联合溶栓可保护血脑屏障受损,降低颅内出血的发生,其作用可能与降低脑组织uPA和uPAR表达以增加CoLIV水平有关。
Cerebral ischemic injury can cause damage to the blood-brain barrier, thrombolytic therapy can re-flow, protect the brain from damage, but can increase intracranial hemorrhage. Naomaitong has been shown to have a protective effect on cerebral ischemic injury. This experiment intends to Naomaitong thrombolysis on the protection of the blood-brain barrier in rats with cerebral ischemia and its possible mechanism of action. The experimental rats were randomly divided into groups; occlusion of the middle cerebral artery of rats by autologous thrombus and thread plug was used to prepare animal model of thromboembolic cerebral ischemia; rats were subjected to thrombolysis through the regional artery 3h, 6h, 9h after ischemia; The changes of intracerebral hemorrhage were observed 24h after treatment, and the expressions of IgG, CoLIV, uPA and uPAR (uPAR) in brain tissue were detected by immunohistochemistry The change. The results showed that the intracerebral hemorrhage rate increased in model group, the level of IgG was increased in 9h and 6h group, CoLIV was decreased, and the expression of uPA and uPAR in each group was significant. The intracranial hemorrhage rate in thrombolytic group was higher than that in model group, , Co-LIV increased and uPA and uPAR expression weakened. Compared with 3h and 6h, the expression of IgG increased, CoLIV weakened and the expression of uPA and uPAR significantly increased. The intracranial hemorrhage rate in combination group was lower than that in thrombolytic group. Respectively, compared with Naomaitong group, CoLIV increased, uPA and uPAR expression weakened. These results suggest that cerebral ischemia can cause the destruction of the blood-brain barrier, thrombolysis can increase the rate of intracranial hemorrhage, Naomaitong combined thrombolysis can protect the blood-brain barrier damage, reduce the occurrence of intracranial hemorrhage, its role may be related to reducing uPA And uPAR expression to increase CoLIV levels.