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Updated: Jan 31, 2026

Stenosis of the Inferior Vena Cava: A Murine Model of Deep Vein Thrombosis
Published on: December 22, 2017
Deep Vein Thrombosis is Modulated by Inflammation Regulated via Sirtuin 1/NF-κB Signalling Pathway in a Rat Model.
Xiaolan Yao1, Wenpei Chen1, Jin Liu1
1School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, China.
Sirtuin 1 (SIRT1) activation reduces deep vein thrombosis (DVT) by decreasing inflammation. This study shows SIRT1 may be a therapeutic target for ameliorating DVT, highlighting its anti-inflammatory role in thrombus formation.
Area of Science:
- Vascular Biology
- Inflammation Research
- Thrombosis Studies
Background:
- Inflammation is crucial in thrombus formation.
- Sirtuin 1 (SIRT1) negatively regulates inflammation by deacetylating nuclear factor-kappa B.
- The role of SIRT1-regulated inflammation in deep vein thrombosis (DVT) remains unclear.
Purpose of the Study:
- To investigate the role of SIRT1 in inferior vena cava (IVC) stenosis-induced DVT.
- To determine if SIRT1 activation can attenuate DVT.
Main Methods:
- Rats underwent IVC stenosis to induce DVT.
- Thrombus weight and histopathology were analyzed.
- Serum inflammatory cytokines and protein expressions (SIRT1, acetylated p65, phosphorylated p65, tissue factor) were measured.
- Effects of resveratrol (SIRT1 agonist) and EX527 (SIRT1 inhibitor) were assessed.
Main Results:
- IVC stenosis led to increased thrombus weight, leukocyte infiltration, and inflammatory cytokines.
- SIRT1 expression decreased, while p-p65, Ace-p65, and TF expression increased post-stenosis.
- Resveratrol reduced thrombus weight and inflammation markers, and increased SIRT1 expression.
- EX527 reversed the protective effects of resveratrol.
Conclusions:
- SIRT1 activation mitigates IVC stenosis-induced DVT through anti-inflammatory mechanisms in rats.
- SIRT1 represents a potential therapeutic target for DVT treatment.
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