摘要
目的:探讨氧化应激在小鼠短暂性脑缺血发作中的作用及其病理生理学机制。方法:采用尾静脉注射过氧化物加缺氧诱发的小鼠TIA模型,通过测定血清可溶性P-选择素水平的变化和小鼠症状的出现时间、模型评分,观察血小板激活和替罗非班的干预作用。结果:模型组血清可溶性P-选择素显著高于对照组,分别为(4.19±0.17)ng/ml和(0.82±0.07)ng/ml,替罗非班组与模型组比较无显著差异(P>0.05);替罗非班组小鼠症状的出现时间明显晚于模型组,分别为(4.95±1.19)d和(3.75±1.12)d;症状评分也低于模型组(P<0.05)。结论:氧化应激通过激活血小板,进而诱发微血栓的形成导致小鼠TIA发作;血小板活化后伴随的炎症反应可能也起了一定的作用。
Objective：Investigate the effects and pathophysiological of oxidative stress in transient ischemic attack.Methods：Mice TIA model was established by injection of preoxide and hypoxia.Tirofiban was given by intravenous injection before preoxide and hypoxia.The serum level of soluble P-selectin,time of symptom emerge and stroke score was determined.Results：The serum P-selectin level of the model group was significant higher than that of the normal group[（4.19 ± 0.17）ng/ml vs（0.82 ± 0.07）,P 〈0.05],but there was no significant difference between the model group and the tirofiban group.The average time of symtom imerged was（4.95±1.19）days in the tirofiban group and（3.75±1.12）days in the model group.The difference was significant between the two groups（P 〈0.05）.Stroke score was also lower in the tirofiban group（P〈0.05）.Conclusion：Platelet activation and microthrombus was induced by oxidative stress in mice TIA model.Inflammatory reaction after platelet activation might also contribute to it.
出处
《脑与神经疾病杂志》
2008年第4期350-352,共3页
Journal of Brain and Nervous Diseases
基金
洛阳市科技发展计划(0701015B)
