大鼠急性一氧化碳中毒迟发型脑病模型中Nrf2的动态表达及其作用

大鼠急性一氧化碳中毒迟发型脑病模型中Nrf2的动态表达及
其作用
何林;张奕雯;范星;张益梅;李经伦
【期刊名称】《实用医学杂志》
【年(卷),期】2016(32)18
【摘要】目的：探讨转录因子NF－E2相关因子2（Nrf2）在急性一氧化碳中毒
迟发型脑病（DEACMP）中的作用。

方法：将168只大鼠随机分为空白对照组（BC组）、空气对照组（AC组）、CO中毒组（CO组）。

采用改良式腹腔注射法制备DEACMP 大鼠模型。

按染毒后第1、3、7、14、21、28天分为6个亚组，造模成功后用TUNEL法检测海马CA1区凋亡细胞，免疫组化法及Western Blot 法检测Nrf2蛋白的表达情况。

结果：CO组海马CA1区凋亡指数从第1天开始增多，第7天达峰值（20．20±1．78）后逐渐减少，第28天仍高于BC、AC组，且每个时间点其凋亡指数较 BC、AC 组均显著增高；CO 组大鼠 Nrf2表达从第1天开始增加，第3天达高峰（8．20±1．08），第28天仍维持在较高水平，且
每个时间点均较其余两组明显增加。

结论：Nrf2与细胞凋亡呈线性相关，在DEACMP的发病机制中起双重作用，在染毒后3 d 内，Nrf2快速增高，发挥抗细胞凋亡作用，第7～28天其持续过量表达，很可能又促进了海马锥体细胞的凋亡，是 CO 中毒发展为 DEACMP 的助推因素。

%Objective To study the effects of nuclear factor E2-related factor 2 (Nrf2) in delayed encephalopathy in rats after acute carbon monoxide poisoning. Methods One hundred and sixty-eight rats were randomly divided into three groups: forty-eight rats in the blank control group (BC group), sixty rats in the air control group (AC
group) as well as in the carbon monoxide poisoning group (CO group). The DEACMP model was established by improved intraperitoneal injections. The animals were valuated at 1st ,3rd, 7th, 14th, 21th, 28th day after acute carbon monoxide poisoning. Tunnel method was used to test the pyramidal cell apoptosis in the hippocampal CA1 area. The expression of Nrf2 was tested by immunohistochemical method and Western Blot method. Result In the CO group, the apoptosis index (AI) started to increase from first day and achieved it's peak at the 7th day (20.20 ± 1.78), then began to decrease slowly. The apoptosis index was still higher than that in the other groups at 28th day. And the apoptosis index of the CO group was markedly higher than the other two groups at each time point. The Nrf2 protein started to increase from 1st day in the CO group , reached its peak at 3rd day (8.20 ± 1.08), reduced later, maintained at a high level at 28th day, and expressed significantly higher than other groups at each time point. Conclusions The Nrf2 has a linear correlation with apoptosis , and plays a dual role in DEACMP because it rapidly increased in first three days to against apoptosis. But it continuously has been excessive expressed from 7th to 28th day in promoting the apoptosis of hippocampus pyramidal cells and may be a positive factor in DEACMP.【总页数】5页(P2984-2987,2988)
【作者】何林;张奕雯;范星;张益梅;李经伦
【作者单位】646000 四川省泸州市，西南医科大学附属医院神经内科;646000 四川省泸州市，西南医科大学附属医院神经内科;646000 四川省泸州市，西南医科
大学附属医院神经内科;646000 四川省泸州市，西南医科大学附属医院神经内科;646000 四川省泸州市，西南医科大学附属医院神经内科
【正文语种】中文
【相关文献】
1.大鼠急性一氧化碳中毒迟发性脑病模型中干预剂叔丁基对苯二酚对Nrf2及HO-1表达的影响 [J], 吕霞;吴沙;何林;辜刚凤;彭红艳;李经纶
2.大鼠海马组织小胶质细胞活化水平与急性一氧化碳中毒迟发型脑病的相关性研究[J], 陈超;王宝军;项文平;李月春;郝喜娃;庞江霞;高浩然;谢伟
3.缺氧诱导因子-1α的表达在大鼠急性一氧化碳中毒迟发型脑病中的作用 [J], 余倩;邓楠;朱木林;沈流燕;周莉;李经伦
4.促红细胞生成素在大鼠急性一氧化碳中毒迟发型脑病中的表达及意义 [J], 朱木林;余倩;陈炳达;李经伦
5.吸入法建立急性一氧化碳中毒迟发型脑病大鼠模型 [J], 陈超;王宝军;项文平;李月春;郝喜娃;庞江霞;高浩然;谢伟
因版权原因，仅展示原文概要，查看原文内容请购买。