| 仇 靖,李岩松,王 敏,姚奔驰,郑 军.阻断趋化因子CXCL10对脑缺血再灌注损伤及神经炎症的影响[J].,2020,(1):41-45 |
| 阻断趋化因子CXCL10对脑缺血再灌注损伤及神经炎症的影响 |
| Influence of Blocking CXCL10 on Cerebral Ischemia-reperfusion Injury and Neuroinflammation |
| 投稿时间：2019-04-21 修订日期：2019-05-15 |
| DOI：10.13241/j.cnki.pmb.2020.01.008 |
| 中文关键词: 脑损伤 氧糖剥夺/复氧 CXCL10 神经炎症 |
| 英文关键词: Brain injury OGD/R CXCL10 Neuroinflammation |
| 基金项目:辽宁省自然科学基金项目（2017010825） |
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| 中文摘要: |
| 摘要 目的：探讨趋化因子CXCL10在脑缺血再灌注损伤中对神经炎症的影响。方法：（1）线栓法建立脑缺血再灌注损伤大鼠模型，TTC染色检测梗死面积，Western blot检测CXCL10的表达；（2）建立小鼠神经瘤母细胞N2a氧糖剥夺/复氧（oxygen-glucose deprivation/reoxygenation,OGD/R）模型，通过CXCR3拮抗剂-NBI 74330阻断趋化因子CXCL10表达，Western blot检测CXCL10和CXCR3蛋白的表达；Real-time PCR检测CXCL10、CXCR3以及神经炎症因子TNF-α、IL-1β、IL-2 mRNA的表达。结果：（1）脑缺血再灌注（cerebral ischemia reperfusion injury, CIRI）模型大鼠脑梗死侧CXCR10的表达量显著高于其对侧和假手术组（P＜0.05）；（2）阻断CXCL10使得小鼠神经瘤母细胞N2a中CXCL10、CXCR3以及炎症因子TNF-α、IL-1β、IL-2的表达量均显著降低（P＜0.05）；（3）阻断CXCL10使得小鼠神经瘤母细胞细胞凋亡率降低（P＜0.05）。结论：抑制CXCL10降低了氧糖剥夺模型细胞炎症因子的表达，表明阻断CXCL10可能通过减轻神经炎症在脑缺血再灌注损伤中发挥保护作用。 |
| 英文摘要: |
| ABSTRACT Objective: The aim of this study is to investigate the effect of blocking chemokine CXCL10 on cerebral ischemia reperfusion injury. Methods: (1)Rat model of cerebral ischemia reperfusion injury was established by line plugging method, and the area of the brain infarct was detected by TTC staining, and the expression of chemokine CXCL10 was detected by Western blotting; (2) The Oxygen-glucose deprivation/reoxygenation model of mouse neuroblastoma N2a was established, and chemokine CXCL10 was blocked by CXCR3 antagonist-NBI 74330, and the protein expression of the chemokine and its receptor CXCR3 was detected by Western blotting, and the mRNA expression of them was detected by Real-time PCR, and the mRNA expression of neuroinflammatory factor that refers to TNF-α , IL-1β, IL-2 was detected in the same way as the former. Results: (1) The expression of CXCR10 in the infarcted side of cerebral ischemia reperfusion injury model was significantly higher than that in the contralateral or the sham-operated groups (P<0.05); (2) The mRNA expression levels of CXCL10, CXCR3 and inflammatory factors in N2a of mouseneuroblastoma cells were significantly decreased (P<0.05). (3) The apoptotic rate of mouse neuroblastoma cells was decreased (P<0.05) after chemokine CXCL10 was blockedby its antagonist. Conclusion: After inhibiting the expression of CXCL10, theexpression of inflammatory cytokines in Oxygen-glucose deprivation/reoxygenation model cells reduced, it suggested that blocking CXCL10 may play a protective role in cerebral ischemia reperfusion injury by mitigating neuroinflammation. |
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