期刊文献+

糖皮质激素对内毒素致急性肺损伤大鼠肺组织Fractalkine表达的影响 被引量:5

Effect of Dexamethasone on Expression of Fractalkine in Lipopolysaccharide-induced Acute Lung Injury
暂未订购
导出
摘要 目的动态观察内毒素(LPS)所致急性肺损伤(acutelunginjury,ALI)大鼠肺组织内趋化因子Fractalkine(FKN)的表达变化,及糖皮质激素对其的影响。方法将42只大鼠随机分为空白对照组、模型组(LPS)及地塞米松干预组(DEX),其中LPS组和DEX组再分为1h、2h、4h3个时相组,每组6只,LPS组和DEX组大鼠经尾静脉注射LPS(4mg/kg)建立ALI大鼠模型。采用ELISA、RT-PCR等方法,观察ALI大鼠模型肺组织病理学改变、肺湿干重比值(W/D)及血清TNF-α变化,并检测肺组织FKNmRNA的表达,同时观察地塞米松对上述指标的影响。结果模型组1h、2h与4h3个时相组肺损伤病理改变、肺W/D、血浆TNF-α均明显增高,地塞米松能减轻ALI大鼠肺组织炎症反应、肺W/D值及血清TNF-α水平(P均<0.05)。正常大鼠肺组织FKNmRNA有表达,模型组3个时相亚组肺组织FKNmRNA表达较正常组明显增加(P<0.05),在2h时点达峰值,地塞米松能下调ALI大鼠肺组织FKNmRNA表达(P<0.05)。FKNmRNA的表达量与血清TNF-α水平呈正相关(r=0.674,P<0.05)。结论早期应用地塞米松可降低TNF-α水平,下调肺组织FKNmRNA的表达,这可能是糖皮质激素对内毒素致急性肺损伤实验大鼠保护作用机制之一。 Objective To investigate the effect of dexamethasone on the expression of fractalkine (FKN) in lipopolysaccharide (LPS)-induced acute lung injury(ALl). Methods The rat model of ALI was established by injection of LPS at the dose of 4 mg/kg. 42 Wistar rats were randomly divided into the normal group (n=6), LPS group (n=18), and dexamethasone (DEX) group (n=18), and then the rats in both LPS and DEX groups were divided into three subgroups (1 h, 2 h and 4 h after injection of LPS), respectively. The pathological condition and the wet/dry ratio (W/D) of the lung were observed, and serum TNF-α level, and FKN mRNA of the lung were detected with ELISA and RT-PCR. Results The W/D, serum TNF-α level, and FKN mRNA of the lung were significantly increased in LPS group, compared with those in normal group (all P〈0. 05), but the W/D, serum TNF-α level, and FKN mRNA of the lung in the DEX group were much more decreased than those in the LPS group (all P〈0.05). In addition, the expression of FKN mRNA in the lung tissue positively correlated with the concentration of TNF-α (r = 0. 674, P〈 0. 05). Conclusion The findings suggested that pre-treatment with dexamethasone could inhibit the TNF-α level and prevent the increase of the expression of FKN mRNA, which may be one of the mechanisms by which DEX serves as a protection against LPS-induced lung injury.
出处 《四川大学学报(医学版)》 CAS CSCD 北大核心 2006年第2期250-253,共4页 Journal of Sichuan University(Medical Sciences)
关键词 急性肺损伤 肿瘤坏死因子-α FRACTALKINE 糖皮质激素 Acute lung injury Tumor necrosis factor-α Fractalkine Dexamethasone
  • 相关文献

参考文献10

  • 1Luce JM. Acute lung injury and the acute respiratory distress syndrome. Crit Care Med,1998;26(2):369-376.
  • 2Bone RC. Immunologic dissonance: a continuing evolution in our understanding of the systemic inflammatory response syndrome (SIRS) and the multiple organ dysfunction syndrome (MODS). Ann Intern Med,1996;125(8):680-687.
  • 3Fong AM, Robinson LA, Steeber DA, et al. Fractalkine and CX3CR1 mediate a novel mechanism of leukocyte capture, firm adhesion, and activation under physiologic flow. J Exp Med,1998;188(8):1413-1419.
  • 4Yoneda O, Imai T, Goda S, et al. Fractalkine-mediated endothelial cell injury by NK cells. J Immunol,2000;164(8):4055-4062.
  • 5李琦,钱桂生,张青,龙勇,高正今,汤正才.大鼠急性肺损伤时肺组织激活蛋白-1活性变化的研究[J].中国呼吸与危重监护杂志,2002,1(1):27-30. 被引量:4
  • 6Aggarwal BB, Kohr WJ, Hass PE, et al. Human tumor necrosis factor. Production, purification, and characterization. J Biol Chem,1985;260(4):2345-2354.
  • 7Bazan JF, Bacon KB, Hardiman G, et al. A new class of membrane-bound chemokine with a CX3C motif. Nature,1997;385(6617):640-644.
  • 8Veyradier A, Nishikubo T, Humbert M, et al. Improvement of von Willebrand factor proteolysis after prostacyclin infusion in severe pulmonary arterial hypertension. Circulation,2000;102(20):2460-2462.
  • 9Yoshida H, Imaizumi T, Fujimoto K, et al. Synergistic stimulation, by tumor necrosis factor-alpha and interferon-gamma, of fractalkine expression in human astrocytes. Neurosci Lett,2001;303(2):132-136.
  • 10Chen YM, Lin SL, Chen CW, et al. Tumor necrosis factor-alpha stimulates fractalkine production by mesangial cells and regulates monocyte transmigration: Down-regulation by cAMP. Kidney Int,2003;63(2):474-486.

二级参考文献11

  • 1毛宝龄.深入探讨全身炎症反应的失控与调控[J].中华内科杂志,1997,36(1):3-4.
  • 2Dokter WHA, Koopmans SB, Vellenga E, et al. Effects of IL-10 and IL-4 on LPS-induced transcription factors(AP-1, NF-IL6 and NF-kappa B) which are involved in IL-6 regulation. Leukemia,1996; 10:1308~ 1316
  • 3Wenner CA, Szabo SJ, Murphy tM. Identification of IL-4 promoter elements conferring Th2-restricted expression during T helper cell subset development. J Immunol, 1997; 158: 765~ 773
  • 4Yan SF,Tritto I, Pinsky D, et al. Induction of interleukin 6(IL-6)by hypoxia in vascular cells, central role of the binding site for nuclear factor-IL-6. J Bio Chem, 1995; 270:11463~ 11471
  • 5Bone RC. Immunologic dissonance: A continuing evolution in our understanding of the systemic inflarmatory response syndrome(SIRS) and the multiple organ dysfunction syndrome (MODS).Ann Intern Med, 1996; 125: 680~ 687
  • 6Bone RC. Sir Isaac Newton. Sepsis, SIRS and CARS. Crit Care Med, 1996;24:1125- 1128
  • 7Karin M, Liu Z, Zandi E. AP-1 function and regulation. Curr Opin Cell Biol, 1997;9:240~246
  • 8Manna SK, Aggarwal BB. IL-13 suppresses TNF-induced activation of nuclear factor-kappa B, activation protein-1, and apoptosis. J Immunol, 1998; 161: 2863~ 2872
  • 9Yamasawa H, Ishii Y, Kitamura S. Cytokine-induced neutrophil chemoattractant in a rat model of lipopolysaccharide-induced acute lung injury. Inflammation, 1999; 23: 263~274
  • 10陈德昌,景炳文,杨建东,杨兴易,陈学云,李红江,严鸣.大黄对胃肠动力学影响的基础和临床研究[J].中国危重病急救医学,1997,9(7):411-413. 被引量:166

共引文献3

同被引文献33

引证文献5

二级引证文献27

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