中文摘要：

目的 ：探讨白介素（interleukin,IL）-18对大鼠深静脉血栓（deep vein thrombosis,DVT）模型血栓形成的影响。方法 ：构建IL18-p CDH-GFP、IL18-LMP-sh RNAmir1病毒载体。SD大鼠（n=27）随机均分为3组。过表达组：尾静脉注入IL-18慢病毒过表达载体（IL18-p CDH-GFP,100μl）;抑制组：注入IL-18逆转录病毒抑制载体（IL18-LMP-sh RNAmir1,100μl）;对照组：注入无菌生理盐水（100μl）。注射24 h后,SD大鼠行狭窄法下腔静脉（inferior vena cava,IVC）血栓造模,造模后24 h解剖观察IVC血栓形成情况,并取材称量血栓重量及长度;血栓静脉管壁行实时荧光定量PCR检测IL-18表达情况。结果：IL18-p CDH-GFP、IL18-LMPsh RNAmir1病毒载体的体外细胞实验具备理想的过表达率及抑制率。各组大鼠造模后24 h可见稳定血栓形成。IL-18过表达组的平均成栓长度和重量较IL-18抑制组、对照组明显增加（P〈0.05）,real-time PCR结果显示过表达组中IL-18在大鼠静脉壁表达量明显增加（F=3.784,P〈0.05）。结论：IL-18表达量增加,对大鼠DVT造模后IVC血栓形成有促进作用,而表达减少亦对成栓有影响,其表达状况与深静脉血栓的发生、发展有关,IL-18介导的促炎反应在静脉血栓疾病发病机制中可能起重要作用。

英文摘要：

Objective：To investigate the influence of intedeukin-18（IL-18） on the rat deep vein thrombosis （DVT）. Methods：Viral vectors of IL18-pCDH-GFP/IL18-LMP-shRNAmirl were constructed. SD rats（n=27） were randomly divided into IL-18 overexpression group,IL-18 inhibition group and control group which were injected with 100 μl IL-18 overexpression lentivectors （IL18- pCDH- GFP）,100 μl IL-18 inhibition retroviral vectors （IL18-LMP-shRNAmirl）,100 μl saline,respectively,into the tail vein. All rats＇ inferior vena cavas（IVC） were modeled as ＂stenosis＂ to promote IVC thrombosis after 24 h of injection. The weight and length of IVC thrombosis after 24 h of modeled were investigated,and the expression of IL-18 in the venous wall was measured by real-time PCR assay. Results：IL18-pCDH-GFP and IL18-LMP-shRNAmirl vectors showed the ideal overexpression/inhibition rate in vitro. All groups had stabilized thrombus formation after modeled 24 h. The average length and weight of thrombus in the IL-18 overexpression group were significantly higher than those of other groups（P 〈 0.05）. The level of IL-18 in the overexpression group was remarkably higher than that of other groups in the vessel wall（F=3.784,P 〈 0.05）,which was proved by real-time PCR assay. Conclusion：IL-18 promotes thrombus formation in rats, and inhibition of IL-18 reduces the thrombus formation. IL-18 may be related to the development process of DVT and its proinflammatory effect may play a vital role in the pathogenesis of VTE.