期刊文献+

急性脑梗死患者TLR4 mRNA表达与TNF-α相关性研究 被引量:10

Correlation between TNF-α concentration and TLR4 mRNA expression in patients with acute cerebral infarction
原文传递
导出
摘要 目的观察急性脑梗死患者Toll样受体4(TLR4)mRNA表达及与TNF-α浓度的相关性,初步探讨TLR4在急性脑梗死缺血炎性损伤中的作用,为临床治疗脑梗死提供新的思路。方法分别运用RT-PCR法、ELISA法测定35例急性脑梗死患者的外周血单个核细胞(淋巴细胞、单核细胞)TLR4mRNA表达及血清TNF-α浓度,同期与20例正常者、20例动脉粥样硬化患者比较。结果脑梗死组发病第三天TLR4mRNA表达、血清TNF-α浓度均显著高于正常对照组和动脉粥样硬化组(P<0.01)。TLR4mRNA表达与血清炎性因子TNF-α浓度呈正相关(P<0.01)。结论脑梗死患者急性期外周血单个核细胞TLR4mRNA表达上调,可能通过促使炎性因子产生分泌增多来介导脑缺血炎性损伤。 Objective To study the correlation between the mRNA expression of Toll-like receptor 4 (TLR4) and the concentration of TNF-α in acute cerebral infarction, in order to explore primarily the role of TLR4 in the inflammatory injury of acute cerebral infarction, and provide a new way for the management of acute cerebral infarction. Methods RT-PCR and ELISA were respectively used to measure the mRNA expression of TLR4 in the peripheral lymphocytes and monocytes, the concentration of TNF-α in the serum. Results The mRNA expression of TLR4 and the concentration of TNF-α in infarction group were significantly higher than those of atherosclerotic group and healthy group at the 3rd day after acute cerebral infarction onset (P〈0.01), and the expression of TLR4 mRNA was correlated positively with the concentration of TNF-α (P〈0.01). Conclusion The expression of TLR4 mRNA in the peripheral lymphocytes and monocytes during acute cerebral infarction are elevated, which may play a critical role in the mechanism of cerebral inflammatory injury through spuring the excretion of inflammatory factor TNF-α.
出处 《中华神经医学杂志》 CAS CSCD 2006年第2期149-151,共3页 Chinese Journal of Neuromedicine
关键词 脑梗塞 TOLL样受体4 肿瘤坏死因子Α 炎性损伤 Brain infarction Toll-like receptor 4 Tumor necrosis factor-α Inflammatory injury
  • 相关文献

参考文献2

二级参考文献44

  • 1李英杰,李达,武晓玲,王振金.脑出血患者血与脑脊液肿瘤坏死因子含量变化的研究[J].脑与神经疾病杂志,1996,4(3):170-171. 被引量:9
  • 2韩玉昆.新生儿缺氧缺血性脑病诊断依据和临床分度[J].中华儿科杂志,1997,35(2):99-100. 被引量:2786
  • 3Kaiser E, kuzmits R, Pregant P, et al. Clinical biochemistry of neuron specificenolase[J]. Clin Chim Acta, 1989, 183 (1): 13-32.
  • 4Nara T, Nozaki H, Nakae Y, et al. Neuron-specific enolase in comatose children[J].Am J Dis Child, 1988, 142 (2): 173-174.
  • 5Liu T, Clark RK, Mc Donnell PC, et al. Tumor necrosis factor-α expression inischemic neurons[J]. Stroke, 1994, 25 (7): 1481-1488.
  • 6Szaflarski J, Burturm K, Silverstein FS. Cerebral hypoxic-ischemia stimulatescytokine gene expression in perinatal rats[J]. Stroke, 1995, 26 (6): 1093-1100.
  • 7Hartmut Jaeschke.Mechanisms of reperfusion injury after warm ischemia of the liver[J]. Journal of Hepato - Biliary - Pancreatic Surgery . 1998 (4)
  • 8Serracino IF,Habib NA,Mathie RT.Hepatic ischemia-reperfusion injury. The American Journal of Surgery . 2001
  • 9Yoshimitsu Kojima,Shohachi Suzuki,Yasuo Tsuchiya,Hiroyuki Konno,Satoshi Baba,Satoshi Nakamura.Regulation of pro-inflammatory and anti-inflammatory cytokine responses by Kupffer cells in endotoxin-enhanced reperfusion injury after total hepatic ischemia[J]. Transplant International . 2003 (4)
  • 10Lentsch AB,Yoshidome H,Cheadle WG,Miller FN,Edwards MJ.Chemokine involvement in hepatic ischemia/reperfusion injury in mice: roles for macrophage inflammatory protein-2 and KC. Hepatology . 1998

共引文献24

同被引文献82

引证文献10

二级引证文献55

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