依达拉奉预处理对大鼠全脑缺血/再灌注损伤的保护作用

目的研究依达拉奉预处理对大鼠全脑缺血/再灌注损伤(I/R)大脑的保护作用,探讨其脑保护作用的可能机制。方法采用改良Pulsinelli法制作大鼠全脑I/R模型。依达拉奉(3mg·kg-1)腹腔内注射法进行预处理。35只健康雄性SD大鼠随机分为7组,每组5只:对照组(C)、缺血再灌注损伤组(I)、依达拉奉预处理组(E),根据再灌注时间(1d、3d、5d)I、E组依次分3个亚组。TUNEL法检测大鼠脑组织海马CA1区神经细胞凋亡数、免疫组织化学pv6001染色法检测Bcl-2、Bax及CytC(cytochromec)蛋白表达的变化。结果与相应I各亚组比较,E各亚组海马CA1区神经细胞凋亡数目显著减少;Bax、CytC蛋白的表达显著减少;Bcl-2蛋白的表达显著增加(P<0.05)。结论依达拉奉预处理可能通过调节凋亡相关调控基因Bcl-2、Bax、CytC的表达,明显减轻大鼠I/R的神经细胞凋亡,从而产生脑保护作用。

Protection of Edaravone pretreatment in brain neurons of rats with injury of global cerebral ischemia-reperfusion

OBJECTIVE To study the effects of Edaravone pretreatment in rats with injury of global cerebral isehemia-reperfusion（I/R） and explore mechanisms of the effects. METHODS The modified Pulsinelli method was used to build rat global cerebral I/R injury model. The intraperitoneal injection method was used to carry out Edaravone （3mg. kg-1） pretreatment. 35 healthy male SD rats were randomly divided into 7 groups of five each： control group （C）, ischemia group （I）, Edaravone pretreatment group （E）. According to reperfusion time （ ld, 3d, 5d）, I, E group were respectively divided into three sub-groups further. Neural apoptosis was identified by ter- minal deoxynucleotidyl transferase-mediated Bioton-dUTP nick end labeling （TUNEL）, and immunohistochemistry was used to detect the expression of B-cell leukemia-2 （Bcl-2）, Bax and CytC（cytochrome c） proteins in neurons in cerebral hippocampus CA1 zone. RESULTS Compared with corresponding I sub-groups, significantly decreased number of apoptotic neurons and the Bax, CytC positive expression ceils, while significantly increased number of Bcl-2 positive expression cells were observed in Edaravone pretreatment groups （P 〈 0.05 ） . CONCLUSUION Edaravone pretreatment is able to significantly decrease the apoptosis of brain neurons in SD rats with jury of global cerebral I/R, thereby preventing neuronal apoptosis. The mechariism of their protection might be related to induction of Bcl-2 protein expression and inhibition of Bax prote;n expression and CytC release by Edaravone pretreatment which prevented apoptosis of neurons.