天津医药

• 实验研究 • 上一篇    下一篇

辛伐他汀对创伤性脑损伤大鼠血清及海马NSE表达的影响

靳春杰1,周伟2,江荣才3,张士俊4,杨大伟4   

  1. 1. 天津医科大学总医院（博士在读）,天津市北辰医院神经外科
    2. 天津中医药大学第二附属医院
    3. 天津医科大学总医院
    4. 天津市北辰医院神经外科
  • 收稿日期:2013-05-22 修回日期:2013-08-26 出版日期:2013-12-15 发布日期:2013-12-15
  • 通讯作者: 靳春杰

Effects of Simvastatin on Neurone-Specific Enolase Expression in Rats with Traumatic Brain Injury

JIN Chun jie1,ZHOU Wei 2,JIANG Rong cai3,ZHANG Shi jun4,YANG Da wei4   

  1. 1. General Hospital of Tianjin Medical University,Department of Neurosurgery, Tianjin Beichen Hospital
    2. Second Affiliated Hospital of Traditional Chinese Medicine
    3. General Hospital of Tianjin Medical University
    4. Department of Neurosurgery, Tianjin Beichen Hospital
  • Received:2013-05-22 Revised:2013-08-26 Published:2013-12-15 Online:2013-12-15
  • Contact: JIN Chun jie

PDF (PC)

2664

摘要：  【摘要】  目的  通过观察辛伐他汀对创伤性脑损伤（TBI）大鼠神经元特异性烯醇化酶（NSE）在脑组织和血清中表达的影响，探讨辛伐他汀对大鼠TBI的治疗作用。  方法  8周龄的SD大鼠90只，随机分为假致伤组、对照组、治疗组，每组30只。对照组、治疗组参照改良的Feeney氏自由落体法制造TBI模型。治疗组大鼠于造模前晚及伤后每晚给予辛伐他汀10mg/kg灌胃；对照组及假致伤组同时给予等量淀粉灌胃。3组大鼠分别于伤后3h、12h、24h、3d、7d、14d取5只大鼠的颈总动脉血3mL，ELISA法测定NSE浓度；断头取脑，免疫组化法检测伤侧海马CA3区NSE表达。  结果  （1）ELISA法测定：对照组，伤后3h血清NSE即开始升高，24h至3d达高峰，14d仍高于假致伤和治疗组；治疗组，伤后3h血清NSE水平升高，24h达高峰，3d至7d下降，明显低于对照组，伤后14d接近假致伤组。（2）免疫组化检测：对照组伤后3h伤侧海马CA3区NSE光密度值下降，3d至7d达低谷，14d时仍显著低于假致伤组；治疗组的大鼠伤后3h伤侧海马CA3区NSE光密度值下降，12h至24h达低谷，但明显高于对照组，7d开始回升，14d时接近假致伤组水平。  结论  辛伐他汀可促进TBI后血清NSE水平的下降，提高损伤侧海马神经元的NSE表达，对TBI后大鼠损伤的神经元有保护作用。

关键词: 脑损伤, 神经元特异性烯醇化酶, 辛伐他汀, 大鼠, Sprague-Dawley

Abstract:

[Abstract]   Objective   To study the effect of simvastatin (SIM) on the expression of neuron specific enoalse (NSE) in
rat brain and serum after traumatic brain injury (TBI), and therapeutic effects of SIM on TBI thereof.  Methods   A total of 90 Sprague-Dwalye (SD) rats aged8weeks were randomly divided into sham TBI group, control group and treatment group (n=30). The TBI model was established in control group and treatment group by using Feeney method. Rats in treatment group were fed SIM10mg/kg in the evening pre-injury and in every evening post-injury while those in control group were fed the same dose of starch at the same time. Blood samples (3mL) were collected from carotid atrery in three groups, then rats were sacrificed and brains were collected at different time points (3h,12h,24h,3d,7d and14d post-injury). The serum expressions of NSE were detected by ELISA method. The NSE expressions in hippocampal area CA3were detected with immunohistochemistry.  Results   (1) In control group, the serum NSE level was significantly increased at 3h after injury, reached the peak at 3d, and was still higher than that of sham injury group at14d. In treatment group, the serum NSE level was increased3h after injury, reached the peak at24h, decreased after3d, and was near the sham injury group at14d after injury, but was significantly lower than that of control group. (2) Immunohistochemical detection showed that the NSE optical density values in hippocampal area CA3area were decreased at3h after injury in control group. The optical density values reached the lowest level between3d to7d and were still significantly lower than those of sham injury group at14d. In treatment group the optical density value was decreased at3h after injury, reached the lowest level between12h to24h and rebounded significantly at7d, then at14d up to the level of sham injury group.  Conclusion   SIM can promote the decrease of serum NSE level in TBI rats and increase the NSE expression of hippocampal neurons of injured side, showing protective effects on neuronal damage after traumatic brain injury.

Key words: brain injuries, neuron-specific enolase, simvastatin, Rats, Sprague-Dawley