摘要
目的 :研究阿司匹林对脑缺血再灌注损伤的影响。方法 :实验分为假手术组、对照组 (10 %乙醇 )、ASA10mg/kg组、ASA4 0mg/kg组和ASA16 0mg/kg组。采用线栓法制备短暂性大脑中动脉缺血模型 (缺血 2h ,再灌注 2 2h) ,观察ASA对脑组织中中性白细胞浸润 ,NF -κB活性 ,IL - 1β、TNF -α和ICAM - 1的表达 ,以及脑梗死体积、神经功能缺损。结果 :ASA可抑制核因子NF -κB激活 ;抑制ICAM - 1、IL - 1β和TNF -α的表达 ;减少中性白细胞浸润 ;减小梗死体积积百分比 ,以ASA 10、4 0mg/kg组的作用更明显 ;对 5分制神经功能评分无影响。结论 :①ASA可减轻脑缺血再灌注损伤 ,小剂量的ASA作用效果较好 ;②脑缺血再灌注损伤过程中存在急性炎症反应 ,ASA可抑制脑缺血再灌注损伤过程中的炎症反应 ;③ASA减轻脑缺血再灌注损伤的机制可能与其抑制炎症反应有关 ,然而小剂量的ASA具有较好的疗效 。
Objective:To study the effect of ASA on brain I/R injury in rats. Methods: Sixty male SD rats were randomized in the sham operation,control,ASA 10 mg/kg,ASA 40 mg/kg and ASA 160 mg/kg groups. MCA occlusion was achieved by advancing a nylon filament into the internal carotid artery. After MCA occlusion for 2 hours and reperfusion for 22 hours,the neutrophil infiltration,the activity of NF-κB,the expression of TNF-α,IL-1β and ICAM-1 in brain tissue,the infarct volume and the neurologic deficit were studied. Results: The ASA inhibited the neutrophil infiltration,activity of NF-κB,the expression of ICAM-1,IL-1βand TNF-α,reduced the infarct volume(ASA10 and 40 mg/kg were more efficient),but yielded no effects on neurologic deficit scores. Conclusions: ①ASA reduced the brain I/R injury,which is more efficient with low dose. ②There was an acute inflammation in brain ischemic reperfusion,which could be inhibited by ASA. Such inhibition might give rise to a reduction of brain I/R injury. ③As the treatment efficacy with low dose ASA is more significant,it is suggested that the neuroprotection of ASA is related to the improvement of cerebral blood flow during brain ischemic reperfusion.
出处
《广州医学院学报》
2002年第3期9-12,共4页
Academic Journal of Guangzhou Medical College