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亚低温对颅脑外伤后NMDAR1表达影响研究
The Effect of Hypothermia on the Expression NMDAR1after Traumatic Brain Injury in Rats

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DOI:
作者:
殷玉华,李明,贾锋, 江基尧,徐蔚
Yin yuhua, Li ming, Jia feng, Jiang jiyao, Xu wei
作者单位:
1.作者单位：昆明医科大学附属第二医院神经外科（在读博士 生）。 地 址：云南省昆明市五华区昆瑞路112号。 Email:yinyuhuacn@yahoo.com.cn 2. 作者单位：上海交通大学附属仁济医院神经外科。
1.Department Of Neurosurgery,Renji Hospital Medical school of Shanghai jiaotong University 2.Department Of Neurosurgery , The 2nd Affiliated Hospital Of Kunming Medical University
关键词:
颅脑外伤； 液压伤； NMDAR1；神经保护
Traumatic brain injury; Lateral fluid percussion; NMDAR1; Neruoprotection
摘要:
目的: 探讨创伤性颅脑损伤（TBI）后亚低温治疗对NMDAR1表达影响。方法：54只成年SD大鼠，随机分为3组：实验组，TBI后亚低温治疗（ n=24, T=32°C)；对照组，TBI后常温治疗组（n=24, T=37°C)；假损伤组（n=6, T=37°C)。液压侧方打击装置制作TBI模型，TBI后随即把大鼠部分浸入0°C冰水中制作低温模型，T=32°C维持4h。实验组和对照组分别在损伤后4h，6h，12h和24h，假手术组为24h，分别处死动物，取伤侧海马CA1行RT-PCR和Western blotting分别检测NMDAR1在mRNA 和蛋白水平的表达变化。结果: 大鼠脑液压伤后损伤同侧CA1神经元上NMDAR1 在mRNA和蛋白水平上表达迅速而显著上调（p < 0.01），均在伤后4h上调达其最高水平，而亚低温干预能够明显降低液压伤所致的NMDAR1表达上调（p < 0.05）。结论: TBI后亚低温治疗能够明显降低液压损伤所致的NMDAR1表达上升水平。
Objective： The study was designed to investigate the effect of hypothermia on the expression of NMDAR1 after fluid percussion traumatic brain injury (TBI) in rats. Methods：54 adult male Sprague Dawley rats were randomly assigned to three groups: TBI with hypothermia treatment (32.5±0.5°C), TBI with normothermia (37±0.3°C), and sham injured control. TBI model was induced by fluid percussion TBI device. Mild hypothermia (32±0.5°C) was achieved by partial immersion in a water bath (0°C) under general anesthesia for 4 hours. All the rats were killed at 4, 6, 12and 24h after TBI. The mRNA and protein levels of NMDAR1 in injured hippocampus of each group were measured using RT-PCR and western blot techniques, respectively. Results：In the normothermic group, NMDAR1 levels in injured hippocampus were significantly increased after TBI compared with those of sham injured animals (p < 0.01). In contrast, post-traumatic hypothermia significantly attenuated such an increase. According to the RT-PCR and western blot analysis, the maximum mRNA levels of NMDAR1 was reduced to 72.46%±3.51 of the corresponding values in the normothermic group in injured hippocampus by hypothermia treatment, respectively (p < 0.01), while the respective maximum protein levels of NMDAR1 were reduced to 81.33%±5.50 (p < 0.01). Conclusion： Our data suggests that moderate F-P brain injury would significantly upregulate NMDAR1 expression, while such an increase could be efficiently suppressed by hypothermia treatment.

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