依达拉奉联合甲强龙对大鼠急性脊髓损伤的保护作用

目的探讨依达拉奉与甲强龙联合应用对大鼠急性脊髓损伤神经组织的保护作用。方法选取120只成年SD大鼠,随机分为5组(每组24只):假手术组、急性脊髓损伤组、依达拉奉治疗组(0.3mg/100g)、甲强龙治疗组(3mg/100g)和联合治疗组(依达拉奉0.3mg/100g+甲强龙1.5mg/100g)。采用改良Allen法制作大鼠T10节段急性脊髓损伤模型。应用后肢运动学评分标准(BBB评分)分别于术后1、2、7和14d对各组大鼠进行评分;采用TUNEL法检测各组脊髓损伤组织中神经细胞凋亡率的变化,Western blot法检测各组脊髓损伤组织中凋亡相关蛋白Bcl-2、Bax和Caspase-3的表达水平变化。结果药物治疗各组大鼠的BBB评分均明显高于脊髓损伤组,且脊髓损伤组织中神经细胞的凋亡率以及Bax和Caspase-3的蛋白表达水平均显著降低,Bcl-2的蛋白表达水平显著增高(P<0.05);联合治疗组大鼠的BBB评分明显高于依达拉奉或甲强龙单独治疗组,且脊髓损伤组织中神经细胞的凋亡率以及Bax和Caspase-3的蛋白表达水平均显著降低,Bcl-2的蛋白表达水平显著增高(P<0.05)。结论依达拉奉联合甲强龙抑制大鼠急性脊髓损伤后神经细胞发生凋亡,发挥神经保护作用,同时能够减少甲强龙的使用剂量。

Protective effect of edaravone combined with methylenolone on nervous tissue of rats with acute spinal cord injury

Objective To investigate the protective effect of edaravone(EDA)combined with methylprednisolone(MP)on nervous tissue of rats with acute spinal cord injury(ASCI).Methods 120 adult SD rats were randomly divided into 5 groups(n=24):sham,ASCI group,EDA therapy group(0.3 mg/100 g),MP(3 mg/100 g),and EDA(0.3 mg/100 g)+MP(1.5 mg/100 g).The modified Allen method was used to make the T10 segment ASCI model.The rats were scored on the 1 st,2 nd,7 and 14 th day after operation with the hindlimb kinematics scoring standard(BBB score).The apoptosis rate of neurons was measured by TUNEL,Western blot was used to detect the expressions of Bcl-2,Bax,and Casapse-3 in ASCI tissues.Results The BBB scores were significantly higher,the expression level of Bcl-2 in spinal lesion tissues was elevated,but the apoptosis rate of neuron cells and the expression level of Bax and Caspase-3 were significantly decreased in treatment groups than in ASCI group.The BBB scores of rats in the combined treatment group were significantly improved.The expression level of Bcl-2 in spinal lesion tissues was significantly elevated,the apoptosis rate of neuron cells and the expression level of Bax and Caspase-3 were significantly suppressed in EDA+MP group than in EDA or MP.Conclusion The protective effect of combined EDA with MP on the damage neurons is related to inhibiting the apoptosis of neurons in rats with ASCI.