脂氧素A_4抑制NLRP3炎性体参与其抗脑缺血再灌注损伤  

Lipoxin A_4 Inhibits NLRP3 in Cerebral Ischemia/Reperfusion Injury

作　　者：吴乐[1] 陈芳[2] 黎红华[1] 武强[1] WU Le;CHEN Fang;LI Hong-hua;WU Qiang(Department of Neurology,Wuhan General Hospital of PLA,Wuhan 430070,China;Department of Medical Laboratory,Wuhan General Hospital of PLA,Wuhan 430070,China)

机构地区：[1]中国人民解放军武汉总医院神经内科,武汉430070 [2]中国人民解放军武汉总医院实验科,武汉430070

出　　处：《神经损伤与功能重建》2018年第4期166-168,共3页Neural Injury and Functional Reconstruction

基　　金：武汉市中青年医学骨干人才培养工程

摘　　要：目的:观察脂氧素A_4(LXA_4)对大脑中动脉闭塞再灌注(MCAO/R)模型大鼠缺血脑组织周边区域的NLRP3阳性神经元数量和NLRP3蛋白表达的影响。方法:SD雄性大鼠24只随机分为假手术组、MCAO/R组和LXA_4组,采用线栓法制作MCAO/R模型,LXA_4组大鼠侧脑室注射0.2 mmol/L LXA_45μL;观察各组脑梗死体积、神经行为学评分、病灶周围NLRP3阳性神经元数及NLRP3蛋白表达。结果:LXA_4明显降低了MCAO/R模型大鼠脑梗死体积和神经行为学评分,减少大鼠缺血灶周边NLRP3阳性神经元数量及NLRP3蛋白表达。结论:LXA_4抑制NLRP3炎性体信号通路可能是其抗脑缺血再灌注损伤的机制之一。Objective:To observe the effects of Lipoxin A4(LXA4)in rat models with middle cerebral artery occlusion/reperfusion(MCAO/R)on the number of NLRP3 positive neurons and NLRP3 protein expression in the territory of the ischemic cortex.Methods:Twenty-four adult male Sprague–Dawley rats were randomly divided into sham group,MCAO/R group,and LXA4 group.MCAO/R models were established using an intraluminal filament method.LXA4 group rats were given a 5μL injection of 0.2 mmol/L LXA4 into the lateral ventricles.The infarct volume,neurological deficit scores,number of NLRP3 positive neurons,and NLRP3 protein expression were observed.Results:LXA4 effectively reduced infarct volume and neurological scores in MCAO/R rats.LXA4 also significantly reduced the number of NLRP3 positive neurons and inhibited the expression of NLRP3.Conclusion:These results suggest that the neuroprotective effects of LXA4 on cerebral ischemia/reperfusion injury are likely achieved by inhibiting the NLRP3 inflammasome signal pathway.

关 键 词：脂氧素A4 脑缺血再灌注损伤 NLRP3 

分 类 号：R741[医药卫生—神经病学与精神病学] R741.02[医药卫生—临床医学]