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作 者:刘松岩[1] 王立威[2] 谭东[3] 杨宏[1] 曹小帅[1] 韩雪梅[1]
机构地区:[1]吉林大学中日联谊医院神经内科,吉林长春130033 [2]长春市人民医院 [3]长春市第二医院
出 处:《中国老年学杂志》2011年第4期616-618,共3页Chinese Journal of Gerontology
基 金:吉林省自然科学基金项目(No.200705268);长春市科技计划项目(No.200808608SF14)
摘 要:目的研究自由基清除剂依达拉奉对癫痫持续状态(SE)大鼠海马中多药耐药基因(MDR1)产物P-糖蛋白(P-gp)表达的影响,以探讨自由基清除剂对难治性癫痫(IE)的防治作用。方法成年SD大鼠随机分为对照组、模型组、依达拉奉组。采用氯化锂-毛果芸香碱腹腔注射制备癫痫持续状态模型,经腹腔注射给药,依达拉奉组于造模成功后即刻腹腔注射依达拉奉,2次/d,3 d后断头取海马,免疫组化检测P-gp表达,图像分析测其表达的灰度值。结果模型组P-gp表达明显高于对照组及依达拉奉组(P<0.01)。结论癫痫发作本身可能是IE的成因,依达拉奉通过清除自由基减轻神经元损伤,进而抑制P-gp表达,可能成为防治IE的有效方法。Objective By observing the effect of edaravone (EDA) on multidrug resistance permeability-glycoprotein (P-gp) expression in hippocampus of epileptic rats to explore prevention and treatment of radical scavenger on intractable epilepsy (IE). Methods 30 adult SD rats were randomly divided into control, model [ status epilepticus ( SE ) ] and EDA groups. SE model was established by injected lithium-pilocarpine intraperitoneal, EDA group were injected intraperitonea1,2 times a day. 3 days later ,hippocampus was obtained to observe the changes of P-gp expression by immunol histochemistry. Results P-gp expression in model group was higher than that of control and EDA groups ( P 〈 0. 01 ). Conclusions SE could induce P-gp expression and maybe is one of the causes of IE. EDA could inhibit P-gp expression by removing radical to protect the neuron, and should be a method that can prevent and control intractable epilepsy.
关 键 词:难治性癫痫 P-糖蛋白(P-gp) 依达拉奉
分 类 号:R742.1[医药卫生—神经病学与精神病学]
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