[1]卫杏利,胡治平.沙鼠脑缺血再灌注损伤后Hsp22和c-fos的表达变化[J].卒中与神经疾病杂志,2016,23(06):449-452.[doi:10.3969/j.issn.1007-0478.2016.06.016]
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沙鼠脑缺血再灌注损伤后Hsp22和c-fos的表达变化()
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《卒中与神经疾病》杂志[ISSN:1007-0478/CN:42-1402/R]

卷:
第23卷
期数:
2016年06期
页码:
449-452
栏目:
论 著
出版日期:
2016-12-30

文章信息/Info

文章编号:
1007-0478(2016)06-0449-04
作者:
卫杏利胡治平
046000 山西省长治医学院附属和平医院老年病科(卫杏利); 中南大学湘雅二医院神经内科(胡治平)
关键词:
脑缺血再灌注 Hsp22 c-fos 蒙古沙鼠
分类号:
R743
DOI:
10.3969/j.issn.1007-0478.2016.06.016
文献标志码:
A
摘要:
目的 探讨沙鼠脑缺血再灌注损伤后脑组织中Hsp22和c-fos的表达变化及相应的保护机制。方法 健康雄性蒙古沙鼠制作脑缺血再灌注模型,缺血10 min,再灌注6 h、1、3、7 d。采用HE染色、免疫组织化学染色法观察脑组织的病理变化,Hsp22和c-fos的表达情况。结果(1)HE染色:脑缺血再灌注组根据时间点的不同可见胶质细胞增生、肥大,细胞间质和细胞水肿,神经元坏死;(2)免疫组化:缺血再灌注损伤后Hsp22的表达上调,于第3 d达到高峰,与对照组比较有显著差异(p<0.05),第7 d开始下降但仍高于正常组和假手术组; c-fos在脑缺血再灌注后表达明显增高,于第1 d达到高峰,与对照组比较有显著差异(p<0.05),随后逐渐减少。结论 沙鼠脑缺血再灌注后脑组织Hsp22及c-fos表达上调,推测Hsp22可能通过抑制c-fos的活性而起到凋亡负性调节的作用。

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更新日期/Last Update: 2016-12-20