摘要
目的:探讨蛇毒激肽原酶对脑缺血再灌注大鼠的缺血区脑组织的保护作用及机制.方法:将实验动物随机分为假手术组、生理盐水对照组和治疗组.治疗组在大鼠脑缺血再灌注后8h,腹腔注射蛇毒激肽原酶17.5U/(kg.d),连续注射3d.于术后第3日行神经功能缺失评分(NSS),然后处死大鼠行梗死体积(TTC染色)的计算、缺血区的病理改变(HE染色)的检查以及缺血区神经细胞情况(尼氏染色)的检查,同时检测缺血区NSE,GFAP及vWF的免疫组化情况.结果:在大鼠脑缺血再灌注后8h,给予蛇毒激肽原酶治疗能明显降低大鼠的神经功能缺损,使大鼠的梗死体积变小,病理改变明显减轻,缺血区的尼氏染色结果得到明显的改善.治疗组脑缺血区的NSE,GFAP及vWF免疫组化的阳性细胞增多,与生理盐水对照组比较有明显差异(P<0.05).结论:蛇毒激肽原酶对脑缺血再灌注大鼠的缺血区脑组织有保护作用;促进缺血区神经细胞的再生以及神经胶质细胞、血管内皮细胞增生为其重要机制之一.
AIM： To explore the effect and the mechanism of kallikrein from Agkistrodon aeutus venom to rats of cerebral ischemic-reperfusion. METHODS： All rats were randomly divided into sham operation group, control group of physiological saline and treatment group. The treatment group rats were intraperitoneally administrated with kallikrein at dose of 17.5 U/（ kg ·d） for 3 d. After 3 d, neurological function was appraised; infarct volume was determined, pathology and Nissl＇s staining in ischemic tissue were detected. And the immunohistochemistry of NSE, GFAP and vWF were detected. RESULTS： The delayed application kallikrein from Agkistrodon acutus venom to rats of cerebral ischemic-reperfusion can obviously reduce the loss of neurological function and the infarct volume. It can also relieve the change of pathology and improve the Nissl＇s staining in the ischemic tissue. It can obviously increase the positive cells of NSE, GFAP and vWF immunohistoehemistry. There were obvious statistics difference （ P 〈 0. 05 ） between group B and group C. CONCLUSION： Delayed application kallikrein from Agkistrodon acutus venom to rats of cerebral ischemic-reperfusion has protective effect to cerebral ischemia. The protective mechanisms were advancing neurogenesis, neurogliocyte regeneration and angiogenesis in the ischemic region.
出处
《第四军医大学学报》
北大核心
2009年第20期2136-2139,共4页
Journal of the Fourth Military Medical University
关键词
白眉蝮蛇蛇毒
激肽原酶
脑缺血
Agkistrodon acutus venom
kallikrein
cerebral ischemia
