胰岛素防治大鼠一氧化碳中毒迟发性脑病的实验研究

doi:10.3969/j.issn.1006-7795.2012.02.020

首都医科大学学报 ›› 2012, Vol. 33 ›› Issue (2): 233-237.doi: 10.3969/j.issn.1006-7795.2012.02.020

胰岛素防治大鼠一氧化碳中毒迟发性脑病的实验研究

廖秋菊, 王晶, 秦俭

首都医科大学宣武医院急诊科,北京 100053

收稿日期:2011-08-29 修回日期:1900-01-01 出版日期:2012-04-21 发布日期:2012-04-21
通讯作者: 王晶

Protective effect of insulin on delayed neuropsychologic sequelae after carbon monoxide poisoning in the rat and its mechanisms

LIAO Qiu-ju, WANG Jing, QIN Jian

Department of Emergency, Xuanwu Hospital, Capital Medical University, Beijing 100053, China

Received:2011-08-29 Revised:1900-01-01 Online:2012-04-21 Published:2012-04-21

摘要/Abstract

摘要： 目的观察胰岛素对一氧化碳(carbon monoxide,CO)中毒后迟发性脑病(delayed neuropsychologic sequelae,DNS)大鼠认知功能及脑神经元凋亡的影响,为临床防治一氧化碳中毒后迟发性脑病提供新的思路。方法采用大鼠腹腔注射CO气体法制备模型。将中毒后存活的大鼠采用抽签法随机分为CO中毒模型组,CO中毒模型+胰岛素组。胰岛素组给予1.2 mL胰岛素葡萄糖溶液(2 U/Kg胰岛素、2 g/kg葡萄糖)快速腹腔注入,连续给药7d;模型组、对照组腹腔注射等剂量的0.9%氯化钠注射液,连续7 d。采用Morris水迷宫检测各组大鼠1~5周逃避潜伏期,TUNEL法检测各组大鼠5周神经元凋亡情况。结果腹腔注入CO后,模型组大鼠出现认知功能下降,脑神经细胞凋亡明显;胰岛素组大鼠认知功能改善,脑组织病理损害减轻,细胞凋亡减轻。结论胰岛素能够改善大鼠认知功能,抑制神经元凋亡,改善存活神经元的细胞形态,对大鼠CO中毒后迟发性脑病具有一定的神经保护作用。

关键词: 一氧化碳中毒, 迟发性脑病, 神经细胞凋亡, 胰岛素

Abstract: Objective To determine the effects of insulin on cognitive function and neuronal apoptosis in delayed encephalopathy rat model of carbon monoxide(CO) poisoning. Methods The rat carbon monoxide poisoning model was established with introducing CO into abdominal cavity. Rats were randomly divided into two groups: CO group and RI-treated group , simultaneously administered 2 g/kg of glucose and 2 U/kg of regular insulin(RI) by intraperitoneal injection for 7 days. The learning and memory in delayed encephalopathy rat model of carbon monoxide poisoning were studied by using a Morris water maze from 1~5 weeks. At 5 weeks after CO exposure brains were perfusion-fixed. Neuronal changes were detected by thionine stain, TUNEL stain was used to assess injury. The data were expressed as(x±s ) and analyzed by analysis of variance. A P value less than 0.05 indicated significance. Results The cognitive function and neuronal apoptosis of RI-treated-group were improved as compared with CO group. Conclusion Insulin could inhibit the cell apoptosis and improve the cognitive function. Insulin could protect the nerve functions and alleviate on delayed neuropsychologic sequelae(DNS) after carbon monoxide poisoning.

Key words: carbon monoxide poisoning, delayed neuropsychologic sequelae, neural apoptosis, insulin

中图分类号:

R 749.6+3

廖秋菊;王晶;秦俭. 胰岛素防治大鼠一氧化碳中毒迟发性脑病的实验研究[J]. 首都医科大学学报, 2012, 33(2): 233-237.

LIAO Qiu-ju;WANG Jing;QIN Jian . Protective effect of insulin on delayed neuropsychologic sequelae after carbon monoxide poisoning in the rat and its mechanisms[J]. Journal of Capital Medical University, 2012, 33(2): 233-237.

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胰岛素防治大鼠一氧化碳中毒迟发性脑病的实验研究

Protective effect of insulin on delayed neuropsychologic sequelae after carbon monoxide poisoning in the rat and its mechanisms

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