阿司匹林促进大鼠缺血脑组织脑源性神经营养因子的表达

目的:探讨不同剂量阿司匹林(Asp)对脑缺血/再灌注(CI/RP)损伤大鼠的神经保护作用及其对脑源性神经营养因子(BDNF)表达的影响。方法:采用线栓法建立大鼠大脑中动脉CI/RP模型,对CI/RP后大鼠进行肢体神经功能缺损评分:1~3分的48只大鼠入选。入选大鼠分为对照组、Asp小剂量组(20 mg.kg-1)、Asp中剂量组(80 mg.kg-1)和Asp大剂量组(320 mg.kg-1),于CI/RP术后每日腹腔注射Asp或溶媒,并进行神经功能缺损评分,72 h后处死,测定脑梗死体积和BDNF免疫组化检测。结果:CI/RP后24、48和72 h各Asp组大鼠与对照组相比,神经缺损评分明显降低(P<0.05或P<0.01),梗死灶体积显著减小(P<0.01),缺血区域BDNF表达显著增加(P<0.05或P<0.01)。对BDNF表达的作用Asp大剂量组的作用并不优于Asp小剂量组和中剂量组。结论:Asp可以减少CI/RP大鼠的脑梗死体积;促进内源性BDNF的表达可能是其神经保护的机制之一,Asp对BDNF表达的作用并非随Asp剂量的加大而增强。

Aspirin Mediates Endogenous Brain Derived Neurotrophic Factor Expression Against Focal Cerebral Ischemia in Rat Model

Aim：To investigate the neurorotective effect of aspirin（Asp） on the expression of the brain derived neurotrophic factor（BDNF） after reversible focal cerebral ischemia.Methods：MCA cerebral ischemia/reperfusion（CI/RP） rat model was established with suture occlusion technique.The modeling rats were randomly divided into four groups：one control group and three Asp groups with different doses（low dose：20 mg·kg-1,middle dose：80 mg·kg-1 and high dose：320 mg·kg-1）.Asp was administered intraperitoneally right after CI/RP and the next 2 days respectively.The neurological deficit scores were recorded continuously for four days.The rats were then killed at 72 h after CI/RP,and the whole brain was removed to measure the infarct volume and expression of BDNF by immunohistochemistry.Results：Compared with the control group,individual in Asp groups showed decreased neurological deficit scores（P0.05 or P0.01）,reduced brain infarct volumes（P0.01） and elevated expression of BDNF（P0.05 or P0.01）.Also,the effect of high dose of Asp was not superior to the low or middle dose.Conclusion：Asp could reduce the brain infarct volume and its up-regulation of endogenous BDNF expression might be the one of mechanisms of protective effects after focal cerebral ischemia.