期刊文献+

重型颅脑损伤后TNF-α表达及其与细胞凋亡的关系 被引量:2

The study on the expression of TNF-α after traumatic brain injury and the relationship between it and apoptosis
下载PDF
导出
摘要 目的探讨肿瘤坏死因子-α(TNF-α)在大鼠重型颅脑损伤后各个阶段的表达水平及其与颅脑损伤后细胞凋亡的关系。方法将36只大鼠随机分为实验组与对照组。实验组大鼠制作重型颅脑损伤模型,对照组大鼠予以假手术处理,两组大鼠分别在伤后6、24与72h通过RT-PCR法检测TNF-αmRNA水平、TUNEL法检测细胞凋亡水平。结果重型颅脑损伤后大鼠脑组织TNF-αmRNA水平、细胞凋亡水平均较对照组明显升高,并在伤后24h达到高峰。结论TNF-α可能在颅脑损伤后的细胞凋亡中起了重要的作用,对TNF-α表达的干预可望起到减少神经元凋亡从而保留更多神经功能的目的。 Objective To analyze the expression of TNF- α after severe traumatic brain injury (TBI) in SD rat, as well as the relation between the expression and apoptosis of cell after TBI. Methods Thirty-six SD rats were divided to study group and control group randomly. In study group, the animals were executed at the time of 6h, 24h, and 72h after employing model of severe TBI. And thus the expression of TNF- α mRNA was evaluated through RT-PCR, and apoptosis of cell was evaluated through TUNEL. In control group, the expression of TNF-α mRNA and apoptosis were evaluated through the same way but without employing model of severe TBI. Results After severe TBI, the expression of TNF- α mRNA and apoptosis increased, and the peak showed up 24h after TBI. Conclusion TNF- α probably takes effect on the apoptosis after TBI, and the intervention of expression TNF- α may lead to the less apoptosis.
出处 《浙江医学》 CAS 2008年第10期1076-1078,共3页 Zhejiang Medical Journal
关键词 颅脑损伤 肿瘤坏死因子Α 细胞凋亡 Traumatic brain injury TNF- α Apoptosis
  • 相关文献

参考文献5

二级参考文献22

  • 1Rink A, Fung KM, Trojanowski JQ, et al. Evidence of apoptotic cell death after experiment traumatic brain injury in the rat. Am J Pathol, 1995, 147:1575-1583.
  • 2Rosomoff HL, Kochanek PM, Clark R, et al. Resuscitation from severe brain trauma. Crit Care Med,1996, 24 (2 Suppl):S48-S56.
  • 3Yin XM, Oltvai ZN, Koesmeyer SJ. BH1 and BH2 domains of Bcl-2 are required for inhibition of apoptosis and heterodimerization with Bax. Nature,1994,369:321-323.
  • 4Oltvai ZN, Milliman CL, Korsemeyer SJ. Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death. Cell, 1993, 74:609-619.
  • 5Itai T, Tanaka M, Nagata S. [J].Eur J Biochem, 2001, 268(7):2074-2082.
  • 6BaeyensKJ, DeBondt HL, Raeymaekers A,et al. [J]. Acta Crystallogr D Bid Crystallogr,1999, 55 (Pt 4):772-778.
  • 7Utsumi T,TakeST, TanakaK, etal. [J]. FEBSLett,2001,500 (1-2): 1-6.
  • 8Idriss HT, Naismith JH. [J]. Microsc Res Tech, 2000 , 50(3): 184-195.
  • 9Krueger JM, Fang J, Taishi P et al. [J]. Ann N Y Acad Sci, 1998,856:148-159.
  • 10Matthias G, Gudrun Z, Eva G et al. [J].EMBO J,1999,18 (11):3034-3043.

共引文献65

同被引文献12

引证文献2

二级引证文献11

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部