目的 探討炎性細(xì)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(jì)學(xué)差異的健康志愿者30例作為正常對(duì)照組。運(yùn)用放射免疫分析檢測(cè)血漿IL-6、IL-8及TNF-α水平，用ELISA法檢測(cè)血漿IL-10水平。并對(duì)DVT組內(nèi)細(xì)胞因子水平分別進(jìn)行相關(guān)性分析，探討各細(xì)胞因子之間的關(guān)系。結(jié)果 相對(duì)于正常對(duì)照組，DVT組細(xì)胞因子水平均明顯升高（P均＜0.001）。DVT組內(nèi)相關(guān)性分析，IL-6與IL-8及IL-10之間無相關(guān)性，IL-8與IL-10及TNF-α之間無相關(guān)性； IL-6與TNF-α之間呈正相關(guān)（r=0.383，P＜0.05），IL-10與TNF-α之間呈正相關(guān)（r=0.390，P＜0.05）。結(jié)論 在DVT患者外周血中，均檢測(cè)到血漿細(xì)胞因子的升高，炎性細(xì)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(chǔ)與臨床雜志, 2006, 13(6): 653-655. doi: 復(fù)制
版權(quán)信息： ?四川大學(xué)華西醫(yī)院華西期刊社《中國普外基礎(chǔ)與臨床雜志》版權(quán)所有，未經(jīng)授權(quán)不得轉(zhuǎn)載、改編
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- 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. 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. 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. 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. Eppihimer MJ, Schaub RG. P-Selectin-dependent inhibition of thrombosis during venous stasis [Ｊ].Arterioscler Thromb Vasc Biol， 2000; 20(11)∶2483.
- 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. 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. 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. 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.