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。

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.