文章摘要
吴乐 ,陈芳 ,黎红华 ,武强.脂氧素A4抑制NLRP3炎性体参与其抗脑缺血 再灌注损伤[J].神经损伤功能重建,2018,13(4):166-168
脂氧素A4抑制NLRP3炎性体参与其抗脑缺血 再灌注损伤
Lipoxin A4 Inhibits NLRP3 in Cerebral Ischemia/Reperfusion Injury
  
DOI:
中文关键词: 脂氧素A4  脑缺血再灌注损伤  NLRP3
英文关键词: Lipoxin A4  cerebral ischemia/reperfusion injury  NLRP3
基金项目:武汉市中青年医学 骨干人才培养工程
作者单位
吴乐a ,陈芳b ,黎红华a ,武强a 中国人民解放军武 汉总医院a. 神经内 科b. 实验科 
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中文摘要:
      目的:观察脂氧素A(4 LXA4)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LXA4组,采用线栓法制作MCAO/R模型,LXA4组大鼠侧脑室注射0.2 mmol/L LXA4 5 μL;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:LXA4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:LXA4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。
英文摘要:
      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 5 μL 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.
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