大鼠局灶性脑缺血再灌注病灶及周围区PAI-1表达

目的:探讨大鼠局灶性脑缺血再灌注后病灶及周围区Ⅰ型纤溶酶原激活物抑制剂(PAI-1)的表达与脑微血管结构改变的关系。方法:采用光镜、电镜、免疫组织化学、Westernblot等技术,观察大鼠局灶性脑缺血再灌注不同时期病灶及周围区脑微血管结构改变及PAI-1表达。结果:大鼠局灶性脑缺血再灌注6h、3d组病灶及周围区脑微血管外间隙水肿及出血,脑微血管基底膜大量破坏,同时再灌注6h、1d组PAI-1表达低于正常对照组,密度值分别为0.16±0.43和0.33±0.61,与对照组(2.19±1.03)差异显著(P＜0.05)。再灌注后期7d组、14d组脑微血管内皮细胞增生,同时PAI-1表达增加,密度值分别为9.48±1.76和8.61±1.35,明显高于对照组(P＜0.01)。结论:大鼠局灶性脑缺血再灌注病灶及周围区脑水肿及出血以6h至3d最严重。PAI-1表达降低可能是导致脑微血管基底膜破坏的原因之一。再灌注后期PAI-1表达增加可能参与脑微血管的再生。

Expression of PAI-1 in ischemic focus and perifocal areas after 2 hours focal cerebral ischemia with reperfusion in rats

AIM: To investigate the relation between the changes of the cerebral microvasculature and the expression of plasminogen activator inhibitor-1 (PAI-1) in ischemic focal and perifocal areas after 2 hours focal cerebral ischemia with reperfusion in rats. METHODS: The changes of cerebral microvascular structure were observed by optical microscope and electric microscope, the expression of PAI-1 were assessed by immunohistochemical staining, Western blotting in ischemic focus and perifocal areas after focal cerebral ischemia with reperfusion. RESULTS: The edema of extra-cellular matrix and the hemorrhage of extravessels in ischemic focus and perifocal areas were most severe, and degradation and the defect of basement membrane were also observed after 6 hours and 3 days reperfusion following focal cerebral ischemia. The expression of PAI-1 decreased significantly compared with control group (P<0.05). CONCLUSION: The decrease in PAI-1 expression in early reperfusion may be main cause to induce damage of cerebral microvascular structure.