Abstract
Background: The present study was designed to explore the regulatory mechanisms and influences of cotinine on deep vein thrombosis (DVT) in rats via the toll-like receptor 4/nuclear factor κ binding (TLR-4/NF-κB) pathway. Methods: In this experimental study, 30 SD rats were randomly assigned to control group, sham operation group, model group, cotinine (10 μg/kg) group, and model + cotinine (10 μg/kg) group. The thromboxane B2 (TXB2), 6-keto-PGF1α, plasminogen activator inhibitor (PAI), tissue plasminogen activator (t-PA), TLR4, NF-κB, and p65 mRNA and protein expression and tissue changes were analyzed by ELISA, Hematoxylin–Eosin (HE) staining, RT-PCR, and Western blot. Results: There was no significant difference between the control and sham operation groups (P>0.05). The model and cotinine groups showed significantly higher mRNA and protein levels of TXB2, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), PAI, TLR-4, and NF-κB, and significantly lower levels of 6-keto-PGF1α and t-PA than the control and sham operation groups (P<0.05), and the model + cotinine group showed significantly higher mRNA and protein levels of TXB2, IL-6 and TNF-α, PAI, TLR-4, and NF-κB and significantly lower levels of 6-keto-PGF1α and t-PA than the model group (P<0.05). Conclusion: Cotinine can aggravate thrombus and inflammation in rats with DVT, and the mechanism may be associated with the activation of the TLR-4/NF-κB inflammatory signaling pathway.
Highlights
Deep venous thrombosis (DVT) can give rise to serious cardiovascular disorders [1,2]
There was no significant difference in inflammatory factors between the sham operation group and the control group
There was no significant difference in plasminogen activator inhibitor (PAI) and tissue plasminogen activator (t-PA) levels between the control group and the sham operation group
Summary
Deep venous thrombosis (DVT) can give rise to serious cardiovascular disorders [1,2]. DVT can give rise to further disorders like pulmonary hypertension, repeated thrombosis, post-thrombotic syndrome, and even fatal pulmonary embolism. Surgical treatment may be an option, but it may destroy venous walls and vascular endothelial cells, and thereby increase the risk of thrombosis recurrence and activation of vascular smooth muscle cells, which often leads to poor prognosis and even further aggravates the disease [9,10]. The present study was designed to explore the regulatory mechanisms and influences of cotinine on deep vein thrombosis (DVT) in rats via the toll-like receptor 4/nuclear factor κ binding (TLR-4/NF-κB) pathway. Conclusion: Cotinine can aggravate thrombus and inflammation in rats with DVT, and the mechanism may be associated with the activation of the TLR-4/NF-κB inflammatory signaling pathway
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