摘要
目的：探讨依达拉奉对脑创伤后神经细胞凋亡的影响及其机制。方法：雄性SD大鼠随机分为对照组、创伤组、依达拉奉组，Marmarou’s法建立弥漫性脑创伤模型。H—E染色观察皮质区神经细胞组织形态变化；免疫组织化学法和免疫印迹法检测磷酸化ERK1／2及Bax的表达；原位缺VI末端标记法（TUNEL）检测神经细胞的凋亡，并对大鼠综合运动功能进行评定。结果：与对照组比较，创伤组中皮质区部分神经细胞出现变性坏死和凋亡的改变，磷酸化ERK1／2（1、6、24、48h）和Bax（6、24、48、72h）表达水平增高；神经细胞凋亡数目（6、24、48、72h）增多；大鼠综合运动能力评分下降。与创伤组比较，依达拉奉组中脑组织形态结构损伤程度、磷酸化ERK1／2和Bax表达、神经细胞凋亡数目显著下降；大鼠的运动功能评分升高。结论：依达拉奉通过抑制ERK1／2信号途径活化，进而抑制促凋亡蛋白Bax表达，减少神经细胞凋亡，发挥对弥漫性脑创伤的保护作用。
Objective： To investigate the effect of edaravone on neuron apoptosis and potential mechanisms after traumatic brain injury （TBI）. Methods： Male Sprague-Dawley rats were divided randomly into three groups： a control group, a traumatic group, and an edaravone treatment group. The TBI model was duplicated with Marmarou＇s diffused brain injury meth- od. Morphological changes in the cortex were observed by H-E staining; The ERK1/2 phosphorylation （p-ERK1/2） and Bax were detected by immunohistochemistry and Western blot; The quantities of neuron apoptosis were observed with TUNEL method. Behavioral tests were performed. Results： Compared with the control group, some neurons displayed histopathologic changes of necrosis and apoptosis; The expressions of ERK1/2 phosphorylation （1, 6, 24, 48 h）, Bax （6, 24, 48, 72 h） and the number of apoptotic neurons （6, 24, 48, 72 h） increased in the traumatic group; The neurological scores of behavior were decreased. Compared with the traumatic group, the morphological damage of brain tissue, the expressions of ERK1/2 phosphorylation and Bax, and the number of apoptotic neurons were decreased obviously in the edaravone group; Meanwhile, the neurological scores of behavior were enhanced （P〈0.05）. Conclusion： Edaravone can inhibit ERK1/2 path- way activation, and then down-regulate Pax expression and reduce neuron apoptosis thus to exert the protective effect on se- vere traumatic brain injury.
出处
《解剖学杂志》
CAS
CSCD
北大核心
2010年第1期65-68,72,共5页
Chinese Journal of Anatomy
基金
河北省博士基金（06547008D-7）
中国人事部留学归国基金（2007-17）
关键词
创伤
脑
依达拉奉
细胞外信号调节激酶
凋亡
神经元
trauma
brain
edaravone
extracellular signal-regulated kinases
apoptosis
neuron
