解剖学报

解剖学报 ›› 2014, Vol. 45 ›› Issue (5): 622-626.doi: 10.3969/j.issn.0529-1356.2014.05.007

• 神经生物学 • 上一篇    下一篇

丁苯酞预处理对脑缺血再灌注损伤大鼠神经功能缺损评分、氧化损伤和形态学的影响

纪海茹1 孔令伟1 孔维2 赵淑敏2* 郑小影2陈萌2   

  1. 1. 承德医学院2012级研究生，河北 承德 067000; 2. 承德医学院脊髓损伤与修复研究室，河北 承德 067000
  • 收稿日期:2014-01-24 修回日期:2014-04-13 出版日期:2014-10-06 发布日期:2013-10-06
  • 通讯作者: 赵淑敏 E-mail:zhaoshumin-2008@163.com

Effect of 3-N-butylphthalide pretreatment on the score of neurological deficit, oxidative stress and pathomorphology in rats with cerebral ischemia reperfusion injury

JI Hai-ru1 KONG Ling-wei1 KONG Wei2 ZHAO Shu-min 2* ZHENG Xiao-ying2 CHEN Meng2   

  1. 1. Graduate Students of 2012, Chengde Medical College, Hebei Chengde 067000, China; 2. Laboratory of Spinal Cord Injury and Rehabilitation, Chengde Medical College, Hebei Chengde 067000,China
  • Received:2014-01-24 Revised:2014-04-13 Online:2014-10-06 Published:2013-10-06
  • Contact: ZHAO Shu-min E-mail:zhaoshumin-2008@163.com

摘要：

目的 探讨丁苯酞（NBP）预处理对脑缺血再灌注损伤大鼠神经功能缺损评分、氧化损伤和形态学的影响。方法 90只雄性SD大鼠随机分为假手术组（Sham）、模型组(IR)、NBP预处理低剂量组(NBP Ⅰ)、NBP预处理中剂量组(NBP Ⅱ)和NBP预处理高剂量组(NBP Ⅲ)，每组18只，制造模型前7d开始灌胃给药，1次/d。线栓法制作大脑中动脉栓塞（MCAO）模型，缺血2h 再灌注24h后进行神经功能缺损评分；2,3,-氯化三苯基四氮唑(TTC)染色观察脑组织梗死的情况；苏木素-伊红(HE)染色显微镜下观察脑组织形态学变化；采用羟胺法测定超氧化物歧化酶（SOD）活性，化学比色法测定谷胱甘肽过氧化物酶（GSH-PX）活性，硫代巴比妥酸(TBA)法测定丙二醛（MDA）含量。 结果 (1) Sham组神经功能缺损评分为零，脑组织无梗死情况发生，神经元形态规则，脑组织中SOD、GSH-PX活性和MDA含量正常。(2) 与IR组比较，NBP预处理各组大鼠神经功能评分显著降低(均P＜0.01)，NBPⅠ、Ⅱ、Ⅲ组神经功能评分依次递减(均P＜0.05)。(3) 与IR组比较，NBP预处理各组脑组织梗死体积依次减小(均P＜0.05)，神经元损伤减轻。(4) NBP预处理各组脑组织中SOD、GSH-PX活性明显升高，MDA含量显著减少(P＜0.01)；NBPⅠ、Ⅱ、Ⅲ组SOD、GSH-PX活性依次递增，MDA含量依次递减(均P＜0.05)。结论 丁苯酞预处理可上调SOD、GSH-PX活性，降低MDA含量，减小脑梗死体积，减轻神经元损伤，发挥对脑缺血再灌注损伤大鼠的预防性保护作用。

关键词: 丁苯酞, 预处理, 脑缺血再灌注损伤, 氧化损伤, 苏木素-伊红染色, 大鼠

Abstract:

Objective To investigate the effects of 3-N-butylphthalide (NBP) pretreatment on the score of neurological deficit, oxidative stress and pathomorphology in rats with cerebral ischemia reperfusion injury (CIRI). Methods Ninety male SD rats were randomly divided into sham operation group (Sham group), model group (IR group), NBP pretreatment low dose group (NBPⅠgroup), NBP pretreatment middle dose group(NBPⅡgroup) and NBP pretreatment high dose group(NBPⅢ group), 18 rats per group. Pretreatment was given once a day within 1 week before establishing the model of cerebral ischemia reperfusion injury. The model of middle cerebral artery occlusion(MCAO) was subjected by suture method. The score of neurological deficit was executed after ischemia for 2h and reperfusion for 24h in all the rats. The cerebral infarction was observed by TTC staining. The pathologic change of brain was observed by HE staining under the microscope. Hydroxylamine method was used to detect activity of SOD, chemical colorimetry method was used to measure activity of GSH-PX, and TBA method was used to detect content of MDA.
Results (1) In Sham group, the score of neurological deficit and the percentage of infarction volume were zero, the morphology of nerve cell was regular, and activity of SOD, GSH-PX and content of MDA of brain tissue were normal. (2) Compared with IR group, the score of neurological deficit was significantly reduced in NBP pretreatment groups (all P＜0.01); the score of neurological deficit was decreased progressively in turn in NBP Ⅰ,Ⅱ,Ⅲ group (all P＜0.05). (3) Compared with IR group, the percentage of infarction volume was cut down progressively in turn in NBPⅠ,Ⅱ,Ⅲ group (all P＜0.05), and neuron injury was also induced obviously in NBP pretreatment groups.(4) Activity of SOD, GSH-PX was largely increased, and content of MDA was greatly decreased in NBP pretreatment groups(P＜0.01). Activity of SOD, GSH-PX went up progressively in turn, and contents of MDA were cut down progressively in turn in NBP Ⅰ,Ⅱ,Ⅲgroup (all P＜0.05). Conclusion 3-N-butylphthalide can significantly up-regulate the activity of SOD and GSH-PX, decrease the content of MDA, reduce the percentage of infarction volume, and relieve the damage of nerve cell to preventively protect the rats with cerebral ischemia reperfusion injury.

Key words: 3-N-butylphthalide, Pretreatment, Cerebral ischemia reperfusion, Oxidative stress, HE staining, Rat