摘要
目的研究阿托伐他汀联合尿激酶溶栓对大鼠大脑中动脉急性脑梗死的疗效。方法选择SD大鼠48只,采用血栓栓塞法制备大鼠大脑中动脉急性脑梗死模型,随机分为阿托伐他汀组、尿激酶组、联合治疗组和对照组,每组12只。缺血3h给予阿托伐他汀或生理盐水,缺血4h给予尿激酶或生理盐水治疗。治疗前和缺血24h行神经功能缺损评分,缺血24h取脑行2,3,5-氯化三苯基四氮唑染色检测脑梗死体积。结果与对照组比较,阿托伐他汀组缺血24h神经功能显著改善[(6.5±4.3)分vs(12.5±4.3)分],脑梗死体积明显降低[(13.8±7.5)%vs(30.5±23.4)%,P<0.05]。与阿托伐他汀组比较,尿激酶组和联合治疗组神经功能改善程度及脑梗死体积降低程度更显著(P<0.05)。与尿激酶组比较,联合治疗组神经功能改善、脑梗死体积减小,但差异无统计学意义(P>0.05)。结论阿托伐他汀对脑梗死组织有保护作用,阿托伐他汀与尿激酶联合治疗有进一步提高疗效的趋势。
Objectives To study the effect of combined atorvastatin and urokinase on middle cerebral artery occlusion in rats.Methods Forty-eight SD rats were randomly divided into atorvasta tin treatment group,urokinase treatment group,combined atorvastatin and urokinase treatment group,and control group (12 in each group).A rat middle cerebral artery occlusion model was established by throbo-embolism.The rats were treated with atorvastatin or saline 3 h after ischemia followed by urokinase or saline 4 h after ischemia.Their neurological function dificits were scorded before treatment and 24 h after ischemia.Their ischemic stroke volume was measured 24 h after ischemia with 2,3,5-triphenyl tetrazolium chloride staining.Results The neurological function score was significantly higher and the ischemic stroke volume was significantly smaller in atorvastatin treatment group than in control group (6.5±4.3 vs 12.5±4.3,13.8%±7.5% vs 30.5%±23.4%,P〈0.05)and in combined atorvastatin and urokinase treatment group than in atorvastatin treatment group (P〈0.05).No significant difference was found in neurological function and ischemic stroke volume between urokinase treatment group and combined atorvastatin and urokinase treatment group (P〉0.05).Conclusion Atorvastatin can protect cerebral tissue against ischemia.Combined urokinase and atorvastatin treatment can improve the therapeutic effect for ischemic stroke.
出处
《中华老年心脑血管病杂志》
CAS
2015年第1期87-89,共3页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
基金
北京市科技计划课题(Z131107002213064)
关键词
梗死
大脑中动脉
尿纤溶酶原激活物
降血脂药
模型
动物
infarction, middle cerebral artery
urinary plasminogen activator
antilipemic agents
models, animal