TXNIP activates NLRP3/IL-1β and participate in inflammatory response and oxidative stress to promote deep venous thrombosis.

Increasing evidence indicates that deep venous thrombosis (DVT) is a common peripheral vascular disease. This study aims to investigate the mechanisms of thioredoxin-interacting protein (TXNIP) and nod-like receptor protein 3 (NLRP3) inflammasome in deep venous thrombosis (DVT). A total of 66 Sprague-Dawley (SD) rats were employed to conduct DVT model.

Sulforaphane alleviates lung ischemia‑reperfusion injury through activating Nrf‑2/HO‑1 signaling.

Oxidative stress and inflammation are both involved in the pathogenesis of lung ischemia-reperfusion (I/R) injury. Sulforaphane (SFN) is a natural product with cytoprotective, anti-inflammatory, and antioxidant properties. The present study hypothesized that SFN may protect against lung I/R injury via the regulation of antioxidant and anti-inflammatory-related pathways.

Resveratrol Ameliorates Deep Vein Thrombosis-Induced Inflammatory Response Through Inhibiting HIF-1α/NLRP3 Pathway.

Deep vein thrombosis (DVT) has become a prevalent and increasingly serious problem globally and resveratrol (Res) is a natural antitoxin that inhibits arterial thrombosis. To investigate the effect of Res on DVT and further explore its mechanism, thrombosis was monitored at different time points and the pathological changes occurring in the inferior vena cava (IVC) and lung tissue were observed in Sprague-Dawley rats. The protein expression of HIF-1α and NLRP3 in the IVC and lung tissue and the concentrations of D-dimer (D2D), prothrombin fragment 1 + 2 (F1 + 2), interleukin-1β (IL-1β), caspase-1, and tissue factor (TF) in the plasma were determined.