首页 | 本学科首页   官方微博 | 高级检索  
检索        

亚低温对HIBD新生鼠大脑皮质神经元NSE表达及血糖水平影响的研究
引用本文:李占魁,李瑞林,郭亚乐,苏宝山,黄绍平,周熙惠.亚低温对HIBD新生鼠大脑皮质神经元NSE表达及血糖水平影响的研究[J].中国当代儿科杂志,2002,4(5):361-364.
作者姓名:李占魁  李瑞林  郭亚乐  苏宝山  黄绍平  周熙惠
作者单位:李占魁, 李瑞林, 郭亚乐, 苏宝山, 黄绍平, 周熙惠
基金项目:陕西省自然科学基金项目 (编号 :99SM 5 2 ),西安交通大学科研培植项目资助
摘    要:目的:通过亚低温对新生鼠缺氧缺血脑损伤(HIBD)大脑皮质神经元特异性烯醇化酶(NSE)及血糖水平影响的研究,探讨亚低温对HIBD的保护作用机制。方法:建立新生鼠HIBD标准化动物模型,将其随机分为对照组、31℃亚低温和34℃亚低温干预组及假手术组,应用免疫组化染色观察大脑皮质区NSE阳性神经元数目,并利用微量血糖监测仪测定血糖。结果:缺血缺氧后12 h,24 h亚低温干预组大脑皮质NSE阳性神经元数目均显著低于对照组[31℃亚低温组:(54.3±6.5) vs (82.3±6.0),(34.6±5.6) vs (53.3±5.6),P<0.05 或 0.01;34℃亚低温组:(56.8±7.1) vs (82.3±6.0),(32.9±4.9) vs (53.3±5.6),P<0.05]。缺氧缺血后12 h,24 h 血糖水平[31℃亚低温组:(5.74±1.52),(5.89±1.62) mmol/L;34℃亚低温组:(5.69±1.48),(5.91±1.53) mmol/L]亦显著高于对照组[(3.64±1.22),(4.16±1.54) mmol/L](P<0.01)。31℃亚低温和34℃亚低温干预两组间各个时期大脑皮质区NSE阳性神经元数目及血糖水平差异无显著性(P>0.05)。结论:亚低温可通过抑制神经元内NSE活性及升高血糖水平,对HIBD新生鼠大脑皮质神经细胞起到保护作用。

关 键 词:亚低温  脑缺氧  脑缺血  烯醇化酶  血糖  新生鼠  
文章编号:1008-8830(2002)05-0361-04
修稿时间:2002年2月10日

Effect of Mild Hypothermia on the Activity of Neuron Specific Enolase in Cortical Neurons and Blood Glucose Level in Neonatal Rats with Hypoxic Ischemic Brain Damage
LI Zhan-Kuai,LI Rui-Lin,GUO Ya-Le,SU Bao-Shan,HUANG Shao-Ping,ZHOU Xi-Hui.Effect of Mild Hypothermia on the Activity of Neuron Specific Enolase in Cortical Neurons and Blood Glucose Level in Neonatal Rats with Hypoxic Ischemic Brain Damage[J].Chinese Journal of Contemporary Pediatrics,2002,4(5):361-364.
Authors:LI Zhan-Kuai  LI Rui-Lin  GUO Ya-Le  SU Bao-Shan  HUANG Shao-Ping  ZHOU Xi-Hui
Institution:LI Zhan-Kuai, LI Rui-Lin, GUO Ya-Le, SU Bao-Shan, HUANG Shao-Ping, ZHOU Xi-Hui
Abstract:Objective To study the neuroprotection of mild hypothermia on hypoxic ischemic brain damage (HIBD). Methods The HIBD model rats were randomly assigned into the 31℃ and 34℃ mild hypothermia groups, sham operated group and control group. The number of cortical neuron specific endolase (NSE) positive neurons was assayed using immunohistochemistry and the blood glucose level was detected in the four groups. Results The number of the cortical NSE positive neurons 12 and 24 h after hypoxic ischemia ( 54.3 ± 6.5 ) and ( 34.6 ± 5.6 ), respectively] in the 31℃ mild hypothermia group was significantly lower compared with the control group ( 82.3 ± 6.0 ) and ( 53.3 ± 5.6 ), respectively] (P< 0.01 or 0.05 ). It was also significantly lower in the 34℃ mild hypothermia group at 12 and 24 h ( 56.8 ± 7.1 ) and ( 32.9 ± 4.9 , respectively] compared with the control group (P< 0.01 or 0.05 ). The blood glucose level 12 and 24 h after hypoxic ischemia ( 5.74 ± 1.52 ), ( 5.89 ± 1.62 ) mmol/L, respectively] in the 31℃ mild hypothermia group was significantly higher than that in the control group ( 3.64 ± 1.22 ) and ( 4.16 ± 1.54 ) mmol/L, respectively] (both P< 0.01 ); and so was the 34℃ mild hypothermia group at 12 and 24 h ( 5.69 ± 1.48 ) mmol/L vs ( 3.64 ± 1.22 ) mmol/L; ( 5.91 ± 1.53 ) mmol/L vs ( 4.16 ± 1.54 ) mmol/L] (both P< 0.01 ). No significant difference was found in the number of cortical NSE positive neurons and blood glucose level between the 31℃ and 34℃ mild hypothermia groups. Conclusions Mild hypothermia may have a protective effect on hypoxic ischemic neurons by restraining the NSE activity in cortical neurons and increasing the blood glucose level.
Keywords:Hypothermia  Cerebral ischemia  Cerebral hypoxia  Neuron specific enolase  Blood glucose  Neonatal rat
本文献已被 CNKI 万方数据 等数据库收录!
点击此处可从《中国当代儿科杂志》浏览原始摘要信息
点击此处可从《中国当代儿科杂志》下载免费的PDF全文
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号