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预吸氧对新生鼠宫内脑缺血再灌注损伤的影响 被引量:1

Effect of the preoxygenation on the cerebral ischemia/reperfusion injury in neonatal rats.
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摘要 目的 探讨预吸氧对新生鼠宫内脑缺血再灌注损伤的影响。方法 取孕21d Wistar大鼠制成缺血再灌注损伤模型。另有同样孕鼠分别在30%、50%和90%氧浓度下预吸氧30min后,完成宫内缺血后再灌注模型的制备。取出新生鼠脑组织应用Western印迹分析检测细胞核内核因子(NF)-κB。应用免疫组织化学分析检测诱生型一氧化氮合酶(iNOS)的表达,同时观察脑组织病理变化。结果新生鼠脑组织细胞核内NF-κB的含量在缺血再灌注后增加。与对照组和再灌注1h组比较,50%预吸氧组新生鼠脑组织细胞核内NF-κB的含量降低,而30%预吸氧组和90%预吸氧组NF-κB含量增加,其中90%预吸氧组增加最明显。与对照组相比,再灌注组和90%预吸氧组iNOS的表达增加明显。50%预吸氧组与再灌注1h组相比有显著差异。结论 新生鼠脑缺血再灌注损伤后,NF-κB活化增强诱导iNOS的表达增加是脑损伤的重要因素。高浓度预吸氧加重脑缺血再灌注损伤,而50%预吸氧可能改善其损伤。 Objective To evaluate the preoxygenation on ischemia/reperfusion injury in neonatal rats, Methods Twenty-one-day pregnant Wistar rats were used to make models of ischemia/reperfusion injury, Other 21-day pregnant rats were exposed to preoxygenation (30% ,50% ,90% O2)for 30 minutes, then they were made the same models. All the rats were decapitated and NF-κB in cerebral tissue cell nuclear were detected by western blotting, and iNOS in cerebral tissue were detected by immunohistochemistry. The neonatal rats cerebral tissue was examined by histologic examination. Results The expression of NF-κB in neonatal rats cerebral tissue increased after ischemia/reperfusion injury. Compared with the control group, the expression of NF-κB in neonatal rats cerebral tissue decreased in 50% preoxygenation group, and that increased in 30% and 90 % preoxygenation group, which increased significantly in 90 % preoxygenation group. The expression of iNOS in neonatal rats cerebral tissue increased in the reperfusion group and 90 % preoxygenation group compared with the control group. Conclusion It is an important cerebral injury factor that NF-κB activate iNOS after ischemia/reperfusion injury. High concentration preoxygenation leads to further injury, while 50% preoxygenation could improve ischemia/reperfusion injury.
出处 《中国小儿急救医学》 CAS 2007年第2期143-145,共3页 Chinese Pediatric Emergency Medicine
关键词 缺血再灌注损伤 预吸氧 核因子-ΚB 诱生型一氧化氮合酶 Ischemia/reperfusion injury Preoxygenation Nuclear factor κB Inducible nitric oxide synthase
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