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目的观察人尿激肽原酶对大鼠脑缺血再灌注损伤后脑组织内胶质细胞源性神经营养因子(GDNF)和血小板源性生长因子(PDGF)表达的影响,探讨其神经保护可能的作用机制。方法实验大鼠随机分为假手术组、模型组和实验组,每组8只。模型组和实验组用线栓法制作大鼠大脑中动脉脑缺血再灌注模型;假手术组接受相似手术处理,但是不插入线栓。实验组于再灌注后5 min静脉注射3.5×10~(-3)PNAU·kg~(-1)人尿激肽原酶,给药体积1 m L·kg~(-1);假手术组和模型组正常喂养。用免疫组织化学法和Western blot法检测脑组织中GDNF和PDGF的表达。结果与假手术组相比,模型组的GDNF和PDGF表达明显增高(P<0.05)。与模型组相比,实验组的GDNF和PDGF表达进一步增高(P<0.05)。结论人尿激肽原酶可通过促进神经营养因子的表达而发挥对脑缺血再灌注损伤的保护作用。
Objective To observe the effect of human kallikrein on the expression of glial cell line-derived neurotrophic factor (GDNF) and platelet-derived growth factor (PDGF) in rat brain after cerebral ischemia-reperfusion injury and to explore the possible neuroprotective Mechanism. Methods Experimental rats were randomly divided into sham operation group, model group and experimental group, with 8 rats in each group. Rats in model group and experimental group were subjected to middle cerebral artery occlusion (MCAO) model by thread occlusion. Rats in sham operation group received similar operation but did not insert thread plug. In the experimental group, 3.5 × 10 ~ (-3) PNAU · kg -1 human kallikrein was injected intravenously 5 min after reperfusion, and the administration volume was 1 m L · kg -1. The sham operation group And model group fed normally. Immunohistochemistry and Western blot were used to detect the expression of GDNF and PDGF in brain tissue. Results Compared with sham operation group, the expression of GDNF and PDGF in model group was significantly increased (P <0.05). Compared with the model group, the expression of GDNF and PDGF in the experimental group was further increased (P <0.05). Conclusion Human urokinase can play a protective role in cerebral ischemia-reperfusion injury by promoting the expression of neurotrophic factor.