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目的探讨依达拉奉(edaravone)对脑创伤的保护作用。方法 112只雄性SD大鼠随机分为3组:对照组、创伤组、依达拉奉干预组。Marmarou′s法建立弥漫性脑创伤模型。电镜观察海马区神经细胞形态变化;蛋白印迹(Western-Blot)法检测磷酸化细胞外信号调节激酶1/2(ERK1/2)表达;水迷宫法测试动物学习记忆功能。结果与对照组比较,磷酸化ERK1/2在伤后1～48h表达水平明显增高(P<0.05);学习记忆指标潜伏期明显延长(P<0.05)。依拉达奉干预组磷酸化ERK1/2表达水平在1,6,24与48h分别为(1.29±0.27),(3.48±1.49),(5.39±2.13)和(1.90±0.72),与创伤组比较明显下降(P<0.05);依拉达奉干预组学习记忆指标潜伏期分别为186.8,100.9,70.6,63.5和60.9s,明显短于创伤组(P<0.05)。结论依拉达奉可抑制脑创伤后ERK1/2活化,对脑创伤后学习记忆损害有改善作用。
Objective To investigate the protective effect of edaravone on traumatic brain injury. Methods One hundred and twelve male SD rats were randomly divided into three groups: control group, trauma group and edaravone intervention group. Marmarou’s law to establish diffuse brain injury model. Electron microscopy was used to observe the morphological changes of neurons in the hippocampus. The expression of phosphorylated extracellular signal-regulated kinase 1/2 (ERK1 / 2) was detected by Western blotting and the learning and memory abilities of rats by water maze. Results Compared with the control group, the expression of phosphorylated ERK1 / 2 increased significantly 1 ~ 48 h after injury (P <0.05), and the latency of learning and memory index was significantly prolonged (P <0.05). The expression level of phosphorylated ERK1 / 2 at 1, 2, 24 and 48h were (1.29 ± 0.27), (3.48 ± 1.49), (5.39 ± 2.13) and (1.90 ± 0.72) (P <0.05). The latent period of learning and memory indexes in Elada Feng intervention group were 186.8, 100.9, 70.6, 63.5 and 60.9s respectively, which was significantly shorter than that in trauma group (P <0.05). Conclusion Eradication can inhibit the activation of ERK1 / 2 after traumatic brain injury and improve the learning and memory impairment after traumatic brain injury.