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 |
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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 |
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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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