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为探讨Edaravone对脑创伤的保护机制,本研究观察了Edaravone对弥漫性脑创伤大鼠脑组织磷酸化细胞外信号调节激酶ERK1/2表达变化的影响。114只雄性SD大鼠,随机分为3组:(1)假手术对照组(A组,n=18),(2)创伤组(B组,n=48),(3)Edaravone治疗组(C组,n=48),采用Marmarou’s法建立大鼠弥漫性颅脑损伤模型。伤后1、3、6、24、48和72h,HE染色观察伤后皮质和海马区神经细胞组织形态变化,Western blot法、免疫组化法检测皮质和海马区p-ERK1/2的表达,术后24、48、72h对大鼠神经运动功能和综合运动能力评分。结果显示:光镜下,伤后6、24h即可见B组大脑皮质和海马区神经细胞胞体收缩呈三角形,胞浆嗜色性减弱,核皱缩浓染,细胞周围出现空隙,即神经细胞变性坏死改变,C组上述改变明显减轻;免疫组化与Western blot法结果显示,与A组比较,B组ERK1/2(即p-ERK1/2)活性在伤后1、3、6、24、48h显著增高(P<0.05);与B组比较,C组中p-ERK1/2在6、24及48h显著回降(P<0.05);神经功能与综合运动能力评分在B组中(8.73±1.4,63.8±27.7)明显低于A组(24.00±0.00,278.4±27.7),C组(17.36±1.63,117.6±20.9)显著回升(P<0.05)。本研究表明Edaravone可改善脑创伤后神经功能损伤,其机制与调节脑创伤后ERK1/2信号活化水平有关。
In order to explore the protective mechanism of Edaravone on brain injury, we investigated the effect of Edaravone on the expression of phosphorylated extracellular signal-regulated kinase (ERK1 / 2) in brain of diffuse brain injury rats. 114 male Sprague-Dawley rats were randomly divided into three groups: (1) sham operation control group (group A, n = 18), (2) trauma group (group B, n = 48), (3) Edaravone treatment group C group, n = 48). Marmarou’s method was used to establish diffuse brain injury model in rats. At 1, 3, 6, 24, 48 and 72 hours after injury, the morphological changes of nerve cells in cortex and hippocampus were observed by HE staining. The expression of p-ERK1 / 2 in cortex and hippocampus was detected by Western blot and immunohistochemistry. Score of neurological function and motor ability at 24, 48, 72 h after operation in rats. The results showed that under the light microscope, the cells in the cerebral cortex and hippocampus in group B showed a triangular cell shrinkage at 6 and 24 hours after injury, and their color weakening and nuclear shrinkage were concentrated in the cytoplasm. The changes of necrosis in group C were significantly reduced. The results of immunohistochemistry and Western blot showed that the activity of ERK1 / 2 (p-ERK1 / 2) in group B was significantly higher than that in group A at 1,3,6,24, (P <0.05). Compared with group B, the expression of p-ERK1 / 2 in group C decreased significantly at 6,24 and 48h (P <0.05). The scores of neurological function and comprehensive exercise capacity in group B ± 1.4,63.8 ± 27.7) was significantly lower than that of group A (24.00 ± 0.00,278.4 ± 27.7), and group C (17.36 ± 1.63,117.6 ± 20.9) was significantly increased (P <0.05). This study shows that Edaravone can improve neurological injury after traumatic brain injury and its mechanism is related to the activation of ERK1 / 2 signal after traumatic brain injury.