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目的探讨自由基清除剂依达拉奉(edaravone)对新生鼠高氧肺损伤的治疗作用,为临床防治新生儿高氧肺损伤提供理论依据。方法96只新生鼠随机分组后分别进行高浓度氧(氧体积分数>0.90,简称高氧)、高氧+依达拉奉处理,并设相应对照。于实验3d、7d后检测各组新生鼠支气管肺泡灌洗液(bronchoalveolar lavagefluid,BALF)中丙二醛(MDA)、总超氧化物歧化酶(SOD)活性、TNF-α及肺核因子-κB(NF-κB)水平的变化,,并观察肺组织病理改变。结果高氧3d后BALF中MDA、TNF-α含量明显高于正常对照组(P均<0.01),SOD活性下降(P<0.01),肺组织NF-κB活性上升(P<0.01),病理切片见明显炎性表现;高氧7d后,上述改变进一步加重。依达拉奉干预高氧损伤3d、7d时BALF中MDA、TNF-α含量和肺NF-κB染色强度均显著降低(P均<0.05),SOD活性上升(P<0.05),肺组织炎性表现较轻。结论高氧可导致新生鼠的急性肺损伤,其机制可能与机体氧化/抗氧化失衡和炎症反应有关。依达拉奉对新生鼠高氧肺损伤发挥积极的保护作用。
Objective To investigate the therapeutic effect of free radical scavenger edaravone on hyperoxia - induced lung injury in neonatal rats and provide a theoretical basis for clinical prevention and treatment of neonatal lung injury. Methods 96 newborn rats were randomly divided into high concentration oxygen (oxygen concentration> 0.90, referred to as hyperoxia), hyperoxia + edaravone, and the corresponding control. The levels of malondialdehyde (MDA), total superoxide dismutase (SOD), TNF-α and pulmonary nuclear factor-κB in bronchoalveolar lavage fluid (BALF) (NF-κB) levels, and observe the pathological changes of lung tissue. Results The contents of MDA and TNF-α in BALF were significantly higher than those in normal control group (P <0.01), the activity of SOD decreased (P <0.01) and the activity of NF-κB in lung tissue increased See obvious inflammatory performance; 7d after hyperoxia, the above changes further aggravate. The levels of MDA and TNF-α in BALF and the intensity of NF-κB staining in lung tissue were significantly decreased after edaravone treatment for 3d and 7d (P <0.05), SOD activity (P <0.05) Light performance. Conclusion Hyperbaric oxygen can cause acute lung injury in neonatal rats, and its mechanism may be related to the imbalance of oxidative / anti-oxidant and inflammatory reaction. Edaravone has an active protective effect on hyperoxia-induced lung injury in neonatal rats.