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Data · dataset · 2026

Mechanism of total flavonoids from Bidens pilosa against deep vein thrombosis based on network pharmacology and experimental verification

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This study aims to investigate the anti-deep vein thrombosis (DVT) mechanism of total flavonoids from Bidens pilosa (TFB) based on network pharmacology and experimental validation.

Description

Active compounds and common targets of B. pilosa against DVT were screened by network pharmacology, followed by protein-protein interaction network analysis, GO and KEGG enrichment analyses, and molecular docking to predict core targets and related pathways.

A mouse DVT model was established using the inferior vena cava stenosis method, and the mice were assigned to the sham, model, low-, medium-, and high-dose TFB, and MK-2206 groups. ELISA, immunohistochemistry, and Western blotting were used to detect inflammatory factors, markers of neutrophil extracellular traps (NETs), and pathway-related protein expression, respectively. Normal mice were additionally assigned to the control, low-, medium-, and high-dose TFB, and warfarin groups, and the effects of TFB on prothrombin time (PT), activated partial thromboplastin time (APTT), and tail bleeding parameters were assessed.

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A total of 4 active compounds and 118 common B. pilosa-DVT targets were identified. Interleukin-6 (IL-6), tumor necrosis factor (TNF), protein kinase Bα (AKT1), IL-1β, and tumor protein p53 (TP53) were predicted as representative core targets. Molecular docking showed that the active compounds had potential binding affinities with these targets.

In vivo experiments showed that TFB reduced thrombus weight and length, decreased plasma D-dimer levels, downregulated IL-6, TNF-α and NET markers, and inhibited phosphorylation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway proteins compared with the model group. In addition, PT, APTT, and tail bleeding parameters in TFB-treated normal mice showed no significant differences compared with the control group.

These results suggest that TFB alleviates thrombus burden in DVT mice, possibly by regulating inflammatory responses, NET formation, and PI3K/AKT signaling activation.

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