Effect of human recombinant prourokinase(rhpro-UK) on thromboembolic stroke in rats

医学 生理盐水 冲程(发动机) 脑出血 重组DNA 组织纤溶酶原激活剂 栓塞 重组组织纤溶酶原激活剂 麻醉 尿激酶 病变 内科学 胃肠病学 病理 缺血性中风 化学 蛛网膜下腔出血 缺血 生物化学 工程类 改良兰金量表 基因 机械工程
作者
Chunyan Hao,Wen-Xia Ding,Qian Sun,Xinxin Li,Wei‐Ting Wang,Zhuan‐you Zhao,Tang Li-da
出处
期刊:European Journal of Pharmacology [Elsevier BV]
卷期号:818: 429-434 被引量:7
标识
DOI:10.1016/j.ejphar.2017.11.026
摘要

We evaluated the efficacy and safety of human recombinant prourokinase ( rhpro-UK) on thromboembolic stroke in rats. 60 rats with thromboembolic stroke were divided into 6 groups (n = 10). The model group was given saline, the reagent groups were given rhpro-UK (5, 10, 20 × 104 U/kg), and positive control groups were given urokinase (UK) 10 × 104 U/kg and recombinant tissue plasminogen activator (rt-PA) 9 mg/kg through intravenous infusion at 1.5 h after embolism. And other 10 rats without occluded by autologous blood clots as the sham group were given saline. At 6 h after treatment, neurological deficit score and Magnetic Resonance Imaging(MRI) including T1WI and T2WI sequence scanning were measured. At 24 h after treatment, the brain was cut for 2,3,5-triphenyltetrazolium chloride (TTC) staining and aspectrophotometric assay to measure the infarct area and intracerebral hemorrhage after neurological deficit detection. rhpro-UK (5, 10, 20 × 104 U/kg) improved neurological disorder by 39.1 ± 19.7% (n = 10, P > 0.05), 65.2 ± 14.2% (n = 10, P < 0.01) and 65.2 ± 14.2% (n = 10, P < 0.01) maximally; decreased brain lesion volume by 36.7 ± 34.8% (n = 10, P < 0.05), 77.6 ± 7.7% (n = 10, P < 0.01) and 80.5 ± 6.9% (n = 10, P < 0.01); decreased infarction area by 38.2 ± 24.0% (n = 10, P < 0.01), 73.9 ± 5.2% (n = 10, P < 0.001) and 79.7 ± 4.0% (n = 10, P < 0.001) respectively, and there were no statistics difference between rhpro-UK (5, 10, 20 × 104 U/kg) and each positive groups at intracerebral hemorrhage (P > 0.05). Rhpro-UK improved the damaged neural function, decreased the extent of the disease and did not raise bleeding, had protective effects for cerebral ischemia in rats.
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