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内毒素对心肌组织核因子-κB活化的影响及其意义 被引量:3

Effects of endotoxin on the activation of nuclear factor-kappaB in myocardium and its significance
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摘要 目的通过观察内毒素(LPS)攻击大鼠心肌组织核因子-κB(NF-κB)的活化情况,探讨心肌损伤的可能信号机制。方法大鼠腹腔注射5mg/kgLPS制作脓毒症模型,采用凝胶阻滞迁移分析法(EMSA)检测心肌组织NF-κB活化情况,RT-PCR法检测TNF-α基因表达情况。结果LPS攻击后1h,NF-κB活化及TNF-α基因表达开始升高,2h达高峰,6h后逐渐下降。相关分析表明,心肌组织NF-κB活化与TNF-α基因表达呈显著正相关(r=0.9922,P<0.05)。结论LPS可增强心肌组织NF-κB的活化并诱导TNF-α基因表达。NF-κB活化导致的TNF-α合成增加在LPS介导心肌损害的分子机制中可能具有重要作用。 Objective To investigate the effects of endotoxin on the activation of nuclear factor-kappaB in myocardium, and to explore the molecular mechanism of acute myocardial injury. Methods Forty male Wistar rats were randomly divided into normal control group (n=10), lipopolysaccharide (LPS) lh, 2h, 6h groups (n=10 for each group). In the latter two groups, LPS was injected into the peritoneal cavity. Tissue samples from the myocardium were collected to determine NF-κB activation by electrophoretic mobility shift assay (EMSA), and the mRNA expression of TNF-α was measured by semi-quantitative reverse transcription polymerase chain reaction (RT- PCR) with GAPDH as internal standard. Results The activation of NF-κB (2. 173± 0. 063) and TNF-α mRNA expression (0. 292± 0. 031) could be detected in myocardium in very low values in normal control group rats, while both the activation and expression were upregulated markedly after LPS challenge, and peaked 2 hours afterwards (37. 793±4. 785 and 1. 182±0. 146, respectively). They were down-regulated (17. 910±3. 791 and 0. 901±0. 128, respectively) 6 hours after LPS challenge. Compared to normal controls, both NF-κB activity and TNF-α mRNA expression were significantly elevated at various time points following LPS stimulation (all P〈0. 01). The activity of NF-κB was positively correlated with TNF-α mRNA expression level in myocardium (r=0. 992 2, P〈0. 05). Conclusions LPS could lead to up-regulation of NF-κB activation in myocardium. The activation of NF-κB results in TNF-α mRNA expression and release. NF-κB signal pathway might play a critical role in the molecular mechanism of LPS induced myocardial injury.
出处 《解放军医学杂志》 CAS CSCD 北大核心 2007年第5期423-424,共2页 Medical Journal of Chinese People's Liberation Army
基金 国家自然科学基金资助课题(30371390 30200293)
关键词 NF-ΚB 肿瘤坏死因子 内毒素类 心肌 NF-kappaB tumor necrosis factor endotoxins myocardium
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  • 1杜晓辉,姚咏明,李荣,申传安,尹会男.脓毒症大鼠肝脏组织Toll样受体4和髓样分化蛋白-2基因表达的变化规律[J].解放军医学杂志,2005,30(10):870-872. 被引量:5
  • 2Yamamoto Y,Gaynor RB.Therapeutic potential of inhibition of the NF-κB pathway in the treatment of inflammation and cancer.J Clin Invest,2001,107(2):135
  • 3Christman JW,Sadikot RT,Blackwell TS.The role of nuclear factor-κB in pulmonary diseases.Chest,2000,117:1482
  • 4Horton JW,Maass DL,White J,et al.Hypertonic saline-dextran suppresses burn-ralated cytokine secretion by cardiomyocytes.Am J Physiol Heart Circ Physiol,2001,280(4):1591
  • 5Zund G,Dzus AL,Pretre R,et al.Endothelial cell injury in cardiac surgery:salicylate may be protective by reducing expression of endothelial adhesion molecules.Eur J Cardiothorac Surg,1998,13:293
  • 6姚咏明,姚胜,陈劲松,李红云,董宁,于燕,盛志勇.NF-κB抑制剂对烫伤脓毒症大鼠致炎/抗炎细胞因子表达的影响[J].解放军医学杂志,2004,29(1):33-35. 被引量:9

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