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高血压性大鼠脑出血后核因子-κB表达的变化 被引量:5

Expression of NF-κB after hypertensive intracerebral hemorrhage in rats
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摘要 目的观察高血压性大鼠脑出血后血肿周围组织核因子-κB(NF-κB)的表达,分析其与出血时间的关系。方法取成年SD大鼠80只,体质量250~300g,大鼠高血压性脑出血模型采用双侧肾动脉前支部分热凝,立体定位仪下自体血脑内注入法建立。随机分为对照组和脑出血组,采用电泳迁移率改变分析方法(EMSA)检测核内NF-κB的活性,用免疫组化方法观察NF-κB在细胞内的表达情况。结果大鼠高血压性脑出血后1h后NF-κB即开始表达,24h达到高峰,持续至72h开始下降。结论高血压性脑出血后早期即有NF-κB的表达,并参与了脑出血后周围脑组织的继发性损伤。 Objective To investigate the expression of nuclear factor-κB (NF-κB) after hy- pertensive intracerebral hemorrhage at different times in rats, and explore the relation between NF-κB to haematoma and time. Methods Adult Sprague-Dawley rats 80, weight from 250 g to 300 g, were randomly divided into two groups: control group and cerebral hemorrhage group. The HICH model of rats was induced by injection of auologous blood with stereotactic techniques after partial coagulation of the anterior branches of bilateral renal arteries. The activity of NF-κB was detected by electrophoretic mobility shift assay and immunohistoehemical methods. Results The activity of NF-κB was higher in the cerebral hemorrhage group than in the control group. Compared with the control group, the expres- sion of NF-κB increased 1 h after in the cerebral hemorrhage group and reached maximum in 24 hours , and decreased in 72 hours. Conclusion The expression of NF-κB rises immediately after intracere- bral hemorrhage, and it increases in large hematoma. It relieves the damage of secondary inflammatory reaction after intracerebral hemorrhage which is caused by NF-κB.
出处 《实用临床医药杂志》 CAS 2013年第7期5-7,19,共4页 Journal of Clinical Medicine in Practice
关键词 脑出血 核因子-ΚB 脑损伤 大鼠 cerebral hemorrhage hypertension NF-κB brain injury rats
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参考文献5

  • 1Zhao X. Zhang Y, Strong R, ct a|. Distinct patterns of intrac- erebral Hemorrhage-induced alterations in NF kppaB subunit, iNOS, and COX-2 expression[J]. Neurochem, 2007, 101: 652.
  • 2肖国民,危静.急性脑损伤大鼠脑组织核转录因子-κB活性及肿瘤坏死因子-α表达的变化[J].中国危重病急救医学,2005,17(5):307-308. 被引量:12
  • 3Stover J F, Schoning B, Sakowitz O W, et al. Effects of tacrolimus on hemispheric water content and cerebrospinal fluid levels of glutamate, hypoxanthine, interleukin-6, and tumor necrosis actor-alpha following controlled cortical impact injury in rats[J]. J Neurosurg, 2001, 94: 782.
  • 4Kriz J, Lalancette-Hebert M. Inflammation, plasticity and re- al- time imaging after cerebral ischermia [ J ]. Acta Neu- ropathol, 2009, 117(5): 497.
  • 5Yanagisawa D, Kitamura Y, Takata K, et al. Possible in- volvement of P2X7 receptor activation in microglial neuropro- tection against focal cerebral ischemia in rats[J]. Biol Pharm Bull, 2008, 31(6): 1121.

二级参考文献12

  • 1Ichikawa K,DeGroot L J,Refetoff S,et al.Nuclear thyroid hormone receptors in cultured human fibrobasts:improved method of isolation,partial characterization,and interaction with chromation[J].Metabolism,1986,35:861-868.
  • 2Stover J F,Schoning B,Sakowitz O W,et al.Effects of tacrolimus on hemispheric water content and cerebrospinal fluid levels of glutamate,hypoxanthine,interleukin-6,and tumor necrosis actor-alpha following controlled cortical impact injury in rats[J].J Neurosurg,2001,94:782-787.
  • 3Baeuerle P,Baltimore D.NF-kappa B:Ten years after[J].Cell,1996,87:13-20.
  • 4Bakdwin A S Jr.The NF-κB and IκB proteins:new discoveries and insights[J].Annu Rev Immunol,1996,14:649-683.
  • 5Beg A A,Baldwin A S Jr.The IκB proteins:multifunctional regulators of Rel/NF-κB transcription factors[J].Genes Dev,1993,10:427-433.
  • 6Beg A A,Ruben S M,Schcinman R I,et al.I kappa B interacts with the nuclear localization sequences of the subunits of NF-κB:amechanism for cytoplasmic retention[J].Genes Dev,1992,9:1899-1913.
  • 7Korner M,Rattner A,Mauxion F,et al.A brain specific transcription activator[J].Neuron,1989,3:563-572.
  • 8Nanaka M,Chen X H,Pierce J E S,et al.Prolonged activation of NF-κB following traumatic brain injury in rats[J].J Neurotrauma,1999,16:1023-1034.
  • 9Connor T J,Song C,Leonard B E,et al.An assessment of the effects of central interleukin-1 beta,-2,-6,and tumor necrosis factor-alpha administration on some behavioural neurochemical,endo-crine and immune paramenters in the rat[J].Neuroscience,1998,84:923-933.
  • 10Suzumura A,Ito A,Yoshikowa M,et al.Ibudilast suppresses TNF alpha production by glial cells functioning mainly as type Ⅲ phosphodiesterast inhibition in the CNS[J].Brain Res,1999,837(1-2):203-212.

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