丁苯酞对SOD1^(G93A)转基因鼠脊髓Ferritin表达的影响  

The effect of NBP on the ferritin expression in spinal cord of the SOD1^(G93A) transgenic mice

作　　者：王坤[1] 王舒[1] 刘珊[1] 刘亚玲[1] 

机构地区：[1]河北医科大学第二医院神经内科,河北省神经病学重点实验室,石家庄050000

出　　处：《脑与神经疾病杂志》2014年第1期19-22,共4页Journal of Brain and Nervous Diseases

基　　金：河北省自然科学基金项目(C2011206176)

摘　　要：目的探讨丁苯酞对SOD1G 93A转基因鼠的神经保护作用及其可能的机制。方法选取SOD1G 93A阳性小鼠48只,随机分为丁苯酞组(发病早期及终末期)和安慰剂组(发病早期及终末期),每组12只,观察SOD1G 93A转基因鼠的发病时间和生存期,采用免疫组化和蛋白印迹的方法观察SOD1G 93A转基因鼠腰髓铁蛋白(Ferritin)表达。结果丁苯酞组的发病时间为118.0±2.5d,与安慰剂组的109.5±2.2d相比较,P<0.05;生存时间为138.6±2.3d,与安慰剂组的128.1±2.8d相比较,P<0.05;免疫组化显示:发病初期,安慰剂组Ferritin阳性细胞显示胞浆和胞膜周围均匀着色,丁苯酞组Ferritin仅胞膜周围着色,胞核和胞浆着色不明显;终末期,丁苯酞组与安慰剂组相比,二者的Ferritin在胞核和胞浆均有着色;蛋白印迹显示:发病初期,Ferritin在腰髓表达量的相对值,丁苯酞组为0.81±0.23,与安慰剂组的1.57±0.43相比较,P<0.05;终末期,丁苯酞组为1.45±0.45,与安慰剂组的1.73±0.36相比较,P>0.05。结论丁苯酞延迟ALS小鼠的发病时间并延长其生存期,丁苯酞延迟小鼠发病可能与调节铁代谢有关。Objective This experiment was aimed to explore the influnce of NBP on SOD1G93A transgenic mice and its probably protective mechanism.Methods The SOD1G93A gene positive mice were randomly divided into dl-3n-butylphthalide （NBP） group （early onset and end-stage）and placebo group （early onset and end-stage）, and each group was 12, Male and female were equal in each group. We observed the onset time and survival time of SOD IC93A transgenic mice and surveyed the expression of ferritin in lumbar spinal cord of different groups of SODI G93A transgenic mice.Results The onset time in dl-3n- butylphthalide group and placebo group were respectively 118.0 ± 2.5 days and 109.5±2.2 days. Compared with placebo group,the time of onset was delayed by NBP（P〈 0.05）. The survival period in the NBP group was longer than the control （P〈0.05）.The results of immunohistochemistry showed that at the early onset, the cytoplasm and membrane were both colored in the ferritin positive cells in the placebo group,while only membrane were colored in NBP group.At the end-stage, both two were colored in the placebo and NBP group.The results of Western blot showed that the relative value of ferritin in the lumbar spinal cord were respectively 0.81±0.23 and 1.57±0.43 in NBP group and contral group at the early onset, P〈 0.05. At the end-stage, they were 1.45±0.45 and 1.73±0.36 in both two group, P〉0.05.Conclusions NBP can delay the onset time and prolong the survival time of ALS mice. In＇addition,NBP can regulate the iron metabolism at the early stage,which is contributed to the protection at the onset time.

关 键 词：肌萎缩侧索硬化 丁苯酞 SOD1G93A转基因鼠 免疫组化 蛋白印迹 铁蛋白 

分 类 号：R744.8[医药卫生—神经病学与精神病学]