Correlation between the expression of IL‑18 and deep venous thrombosis
- Guangdi Li
- Rudan Zhou
- Xueling Zhao
- Riguang Liu
- Chuan Ye
Affiliations: Department of Orthopedics, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China, Department of Orthopedics, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032, P.R. China
- Published online on: May 16, 2018 https://doi.org/10.3892/ijmm.2018.3682
Copyright: © Li
et al. This is an open access article distributed under the
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The present study aimed to investigate the effect of the expression of interleukin (IL)‑18 and related markers on deep venous thrombosis (DVT) to examine their correlation. Sprague‑Dawley rats of different models were established and were randomly assigned into three groups. The expression of IL‑18, nuclear factor (NF)‑κB and von Willebrand factor (vWF) were detected in blood samples. The inferior vena cava (IVC) was ligated to establish the DVT model. Rat IL‑18 overexpression and inhibition vectors were constructed. The expression levels of IL‑18 and related markers in the venous wall were compared between the model group and the control group using reverse transcription‑quantitative polymerase chain reaction and western blot analyses. Following the culture of human umbilical vein endothelial cells (HUVECs), IL‑18 was added to the cells, following which the growth of the HUVECs, and changes in vWF and other endothelial functional markers were analyzed. The IVC model demonstrated complete thrombosis at 8 h and stable thrombosis at 24 h. At 24 h following model establishment, the expression levels of IL‑18, NF‑κB and vWF were high in the blood samples with the occurrence and development of thrombosis (P<0.05). The weight, length and weight/length ratio of thrombi in each model group showed significant differences from those in the control group (P<0.05) with the overexpression of IL‑18, and the expression levels of NF‑κB and vWF in venous tissues were altered with abnormal expression levels of IL‑18. IL‑18 damaged HUVECs and significantly increased viability in early‑stage apoptosis, promoted the upregulation of vWF and P‑selectin, and reduced tissue plasminogen activator. IL‑18 and the related markers were closely associated with the occurrence and development of DVT.