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目的:观察注射用纤溶酶对大鼠脑缺血再灌注损伤的保护作用,初步探讨其机制。方法:健康成年SD(Sprague Dawley)大鼠30只随机分为假手术组、对照组和给药组,每组10只。参照Nagasawa报道的方法建立脑缺血再灌注动物模型,给药组于再灌注后2h、24h静脉注射纤溶酶,对照组以同样方法注入相同体积的无菌生理盐水。48h后按ZeaLong5分制标准评分进行各组大鼠神经功能评价,免疫组化和HE染色检测大鼠脑内TGF-β1和IL-1β的表达。结果:给药组与对照组相比较,神经功能障碍明显减轻(P<0.01)。与缺血再灌注对照组相比,注射蛇毒纤溶酶,可使脑内TGF-β1表达量增多,IL-1β的表达量减少(P<0.01)。结论:注射蛇毒纤溶酶对脑缺血再灌注有明显的保护作用,IL-1β的表达量减少及TGF-β1表达增多可能是其机制之一。
Objective: To observe the protective effect of plasmin for injection on cerebral ischemia-reperfusion injury in rats and its mechanism. Methods: Thirty healthy adult Sprague Dawley rats were randomly divided into sham-operation group, control group and administration group, with 10 rats in each group. The animal model of cerebral ischemia-reperfusion was established according to the method reported by Nagasawa. The treatment group received intravenous injection of plasmin 2h and 24h after reperfusion, and the same volume of sterile saline was injected into the control group in the same way. After 48h, the neurological function of rats in each group was evaluated by ZeaLong5 score system. The expression of TGF-β1 and IL-1β in rat brain was detected by immunohistochemistry and HE staining. Results: Compared with the control group, the neurological deficit in the treated group was significantly reduced (P <0.01). Compared with the ischemia-reperfusion control group, injection of the venom fibrinolysin increased the expression of TGF-β1 and the expression of IL-1β in the brain (P <0.01). Conclusion: The injection of venom fibrinolytic enzyme has obvious protective effect on cerebral ischemia-reperfusion. The decrease of IL-1β expression and the increase of TGF-β1 expression may be one of its mechanisms.