Background: This study was designed to explore the regulatory mechanisms and influences of cotinine on deep vein thrombosis (DVT) in rats via the toll-like receptors / nuclear factor kappa binding (TLR-4/NF-κB) pathway. Patients and 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 TXB2, 6-keto-PGF, PAI, t-PA, TLR4, NF-κB, and p65 mRNA and protein expression and tissue changes were analyzed by ELISA, 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, IL-6 and TNF-α, PAI, TLR-4, and NF-κB, and significantly lower levels of 6-keto-PGF 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-PGF 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.

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