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实验性脑震荡大鼠脑皮质肿瘤坏死因子-α的表达

严琦敏 张排旗 赵波 张新宇 付学锋

山西医科大学学报Issue(12):1193-1197,5.
山西医科大学学报Issue(12):1193-1197,5.DOI:10.13753/j.issn.1007-6611.2015.12.008

实验性脑震荡大鼠脑皮质肿瘤坏死因子-α的表达

Changes of TNF-αexpression in cerebral cortex of experimental rats with pure cerebral concussion

严琦敏 1张排旗 2赵波 3张新宇 3付学锋3

作者信息

  • 1. 解放军第323医院普通外科,西安 710054
  • 2. 第四军医大学唐都医院消化内科
  • 3. 兰州军区兰州总医院神经内科
  • 折叠

摘要

Abstract

Objective To investigate the changes of tumor necrosis factor-α( TNF-α) in prefrontal cortex( PC) , temporal cortex( TC) and piriform cortex(Pir) after the pure cerebral concussion(PCC), and to explore its relationship with pathological changes in early stage of brain injury. Methods Under the consciousness condition, the PCC model rats were established by a metallic pendulum-striker concussive device. The model rats were randomly divided into 1,12,24,48,72 h and 7 d PCC groups(n=6 in each group), and six normal rats were chosen as control group. The distribution and changes of TNF-α expression in PC,TC and Pir were observed and compared by the immunohistochemistry with anti-TNF-αmonoclonal antibody between PCC groups and control group. Results The expression of TNF-α-immunoreactivity was weak in control group. The expression of TNF-α-immunoreactivity and the number of the TNF-α-immunopositive cells gradually increased from 1 h to 72 h in the PC and TC after the rat brain injury, and peaked at 72 h (P<0. 05 or 0. 01), and then decreased but it was still higher than that in control group at 7 d(P<0. 05). Conclusion The TNF-α expression in PC and TC areas shows obvious changes in PCC rats, suggesting that TNF-αmay be involved in the pathophysiological process of PCC.

关键词

单纯性脑震荡/大脑皮质/TNF-α/免疫组织化学/大鼠

Key words

pure cerebral concussion/cerebral cortex/TNF-α/immunohistochemistry/rats

分类

医药卫生

引用本文复制引用

严琦敏,张排旗,赵波,张新宇,付学锋..实验性脑震荡大鼠脑皮质肿瘤坏死因子-α的表达[J].山西医科大学学报,2015,(12):1193-1197,5.

基金项目

全军医药卫生科研基金资助项目(CLZ11JB02) (CLZ11JB02)

甘肃省自然科学基金资助项目(120RJZA274) (120RJZA274)

兰州军区医药卫生科研基金资助项目(CLZ11JB02) (CLZ11JB02)

山西医科大学学报

OACSTPCD

1007-6611

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