• 四川省瀘州醫(yī)學院附屬醫(yī)院血管外科(瀘州646000);

目的 探討炎性細胞因子IL-6、IL-8、IL-10及TNF-α在急性下肢深靜脈血栓形成(DVT)疾病中的水平及意義。方法 選擇未經(jīng)治療的急性下肢DVT患者40例為DVT組,年齡、性別比無統(tǒng)計學差異的健康志愿者30例作為正常對照組。運用放射免疫分析檢測血漿IL-6、IL-8及TNF-α水平,用ELISA法檢測血漿IL-10水平。并對DVT組內(nèi)細胞因子水平分別進行相關性分析,探討各細胞因子之間的關系。結(jié)果 相對于正常對照組,DVT組細胞因子水平均明顯升高(P均<0.001)。DVT組內(nèi)相關性分析,IL-6與IL-8及IL-10之間無相關性,IL-8與IL-10及TNF-α之間無相關性; IL-6與TNF-α之間呈正相關(r=0.383,P<0.05),IL-10與TNF-α之間呈正相關(r=0.390,P<0.05)。結(jié)論 在DVT患者外周血中,均檢測到血漿細胞因子的升高,炎性細胞因子可能在靜脈血栓形成疾病中起重要的作用。

引用本文: 周翔宇,何延政,何春水,劉勇. 急性下肢深靜脈血栓形成患者IL-6、IL-8、IL-10及TNF-α的水平及意義探討. 中國普外基礎與臨床雜志, 2006, 13(6): 653-655. doi: 復制

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  2. 2.  Fichtlscherer S, Breuer S, Heeschen C, et al. Interleukin-10 serum levels and systemic endothelial vasoreactivity in patients with coronary artery disease [J]. J Am Coll Cardiol, 2004; 44(1)∶44.
  3. 3.  Roumen-Klappe EM, den Heijer M, van Uum SH, et al. Inflammatory response in the acute phase of deep vein thrombosis [J]. J Vasc Surg, 2002; 35(4)∶701.
  4. 4.  Suwa T, Hogg JC, Quinlan KB, et al. The effect of interleukin-6 on L-selectin levels on polymorphonuclear leukolytes [J]. Am J Physiol Heart Circ Physiol, 2002; 283(3)∶H879.
  5. 5.  Min W, Bradley JR, Galbraith JJ, et al. The N-terminal domains target TNF receptor-associated factor-2 to the nucleus and display transcriptional regulatory activity [J]. J Immunol, 1998; 161(1)∶319.
  6. 6.  Eppihimer MJ, Schaub RG. P-Selectin-dependent inhibition of thrombosis during venous stasis [J].Arterioscler Thromb Vasc Biol, 2000; 20(11)∶2483.
  7. 7.  Henke PK, Wakefield TW, Kadell AM, et al. Interleukin-8 administration enhances venous thrombosis resolution in a rat model [J]. J Surg Res, 2001; 99(1)∶84.
  8. 8.  Myers DD Jr, Hawley AE, Farris DM, et al. Cellular IL-10 is more effective than viral IL-10 in decreasing venous thrombosis [J]. J Surg Res, 2003; 112(2)∶168.
  9. 9.  Cassatella MA, Gasperini S, Bovolenta C, et al. Interleukin-10 (IL-10) selectively enhances CIS3/SOCS3 mRNA expression in human neutrophils: evidence for an IL-10-induced pathway that is independent of STAT protein activation [J]. Blood, 1999; 94(8)∶2880.
  10. 10.  van Haelst PL, Tervaert JW, Bijzet J, et al. Circulating monocytes in patients with acute coronary syndromes lack sufficient interleukin-10 production after lipopolysaccharide stimulation [J]. Clin Exp Immunol, 2004; 138(2)∶364.