脂氧素A4抑制NLRP3炎性体参与其抗脑缺血再灌注损伤

摘要

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 LXA4group. MCAO/R models were established using an intraluminal filament method.LXA4group rats were given a 5 μL injection of 0.2 mmol/L LXA4into the lateral ventricles. The infarct volume, neurological deficit scores, number of NLRP3 positive neurons, and NLRP3 protein expression were observed.Results:LXA4effectively reduced infarct volume and neurological scores in MCAO/R rats. LXA4also significantly reduced the number of NLRP3 positive neurons and inhibited the expression of NLRP3.Conclusion:These results suggest that the neuroprotective effects of LXA4on cerebral ischemia/reperfusion injury are likely achieved by inhibiting the NLRP3 inflammasome signal pathway.%目的:观察脂氧素A(4LXA4)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 LXA45 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.