脑外伤后氧化应激对神经细胞凋亡及c-myc蛋白表达的影响

Effect of oxidative stress on neuronal apoptosis and c-myc expression after acute traumatic brain injury

目的 探讨氧化应激对脑损伤后神经细胞凋亡和c -myc蛋白表达的影响及c -myc基因在脑损伤神经细胞凋亡中的作用。 方法 90只SD大鼠液压冲击致脑损伤后 ,随机分成两组 ,实验组给予单甲氧基聚乙二醇 -超氧化物歧化酶 (monomethoxypolyethleneglycolmodified -SOD ,MPEG -SOD) ,对照组给予等渗盐水 ,分别于伤后 3,12 ,2 4 ,4 8,72h采用原位末端标记法 (TdT -med iatedbiotinylated -dUTPnickendlabeling ,TUNEL)检测脑损伤区神经细胞凋亡 ,流式细胞仪检测神经细胞凋亡率 ;免疫组织化学法检测c-myc蛋白的表达。 结果 大鼠脑损伤后 3h ,在实验组和对照组均可检测到神经细胞的凋亡和c-myc蛋白的表达 ,至 2 4～ 4 8h达到高峰。实验组神经细胞凋亡率和c -myc蛋白的灰度明显较对照组低 (P <0 .0 1)。TUNEL阳性细胞数和c -myc蛋白灰度具有明显的相关性 (实验组r=0 .92 ,对照组r =0 .84 ,P <0 .0 1)。 结论 脑损伤后氧化应激诱导神经细胞凋亡和c -myc蛋白表达 ;c

Objective To explore the effect of oxidative stress on neuronal apoptosis and c myc expression and the role of c myc gene in promoting neuronal apoptosis after traumatized brain injury (TBI) in rats. Methods Ninety SD rats were divided into two groups (experimental group and sham group) after fluid percussion. The experimental group was administered with monomethoxypolyethleneglycol modified SOD (MPEG SOD) and the sham group with normal saline. TdT mediated biotinylated dUTP nick end labeling (TUNEL) method was used to detect the neuron apoptosis in the traumatized areas in both groups 3, 12, 24, 48 and 72 hours respectively after operation and flow cytometric analysis to analyze the apoptotic rate of neurons. The expression of c myc protein was detected by immunohistochemistry. Results The neuron apoptosis and the positive expression of c myc protein were detected in both groups 3 hours after trauma and peaked at at the 24 48th hours. The apoptotic rate of neurons and the gray scale of c myc protein in the experimental group were lower significantly than that in the sham group ( P < 0.01 ).There was a remarkable correlation between the TUNEL positive neurons and the gray scale of c myc protein in both groups ( r = 0.92 in the experimental group, r = 0.84 in the sham group, P <0.01). Conclusions The oxidative stress can promote the neuron apoptosis and the expression of c myc protein. At the same time, c myc protein can accelerate the neuron apoptosis after TBI.