Deep vein thrombosis (DVT) is a common
peripheral vascular disease, which may result in
pulmonary embolism and is accompanied by endothelial injury. However, the pathogenesis of DVT remains unclear. Coagulation factor XII (FXII), as an important
coagulation factor, has been reported to be closely associated with
thrombosis. However, the association between FXII
protein and DVT formation is not yet fully understood. The present study examined the effects of FXII
protein on DVT formation and aimed to reveal the underlying mechanism. In the present study, histological characterization of the femoral vein tissue was examined by
hematoxylin and
eosin staining. The damage to the femoral vein tissue was examined by TUNEL assay.
Superoxide dismutase (SOD) and
malondialdehyde (MDA) concentrations were examined using ELISA.
Tumor necrosis factor (TNF)‑α,
interleukin (IL)‑6, IL‑8 and phosphoinositide 3‑kinase (PI3K)/AKT signaling were determined by ELISA, immunohistochemical staining and western blot analysis. The results demonstrated that
thrombosis, FXII
protein, cell apoptosis and the SOD concentrations were decreased, while the MDA concentrations were increased in mice with DVT compared with the control or
sham groups. TNF‑α, IL‑6, IL‑8 and PI3K/AKT signaling was also upregulated in the mice with DVT. Furthermore, the knockdown of FXII significantly upregulated the SOD concentrations and downregulated
thrombosis and cell apoptosis, as well as the MDA concentrations in mice with DVT. The knockdown of FXII also significantly downregulated the
protein expression of TNF‑α, IL‑6 and IL‑8, and the activation of PI3K/AKT signaling. Additionally,
LY294002 pre‑treatment markedly downregulated
thrombosis and cell apoptosis and the MDA content, whereas it upregulated the SOD concentrations in mice with DVT.
LY294002 pre‑treatment also significantly downregulated the TNF‑α, IL‑6 and IL‑8
protein levels. Taken together, the present study demonstrates that FXII
protein promotes DVT via the activation of PI3K/AKT signaling by inducing an inflammatory response. Targeting FXII
protein may thus prove to be a potential approach for the treatment of DVT.