ArticleRespiratory research2025
Sodium butyrate targets VWF to inhibit cigarette smoke extract-induced endothelial cell-macrophage crosstalk in regulating inflammatory response.
Article in Respiratory research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Butyrate Regulating Inflammatory Responses in Chronic Obstructive Pulmonary Disease via the Gut-Lung Axis.International journal of chronic obstructive pulmonary disease · 2026Review
- From the gut to the lungs: The role of gut microbiota in chronic obstructive pulmonary disease and related research progress.Microbial cell (Graz, Austria) · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
Previous studies have shown that cigarette smoke-induced inflammation is a key driver of chronic obstructive pulmonary disease (COPD) progression. Sodium butyrate (NaB), a short-chain fatty acid that can be endogenously produced or exogenously supplemented, has been reported to exhibit anti-inflammatory effects. This study investigated the therapeutic effects and mechanisms of NaB in cigarette smoke extract (CSE)-induced inflammation. Through network pharmacology analysis, von Willebrand factor (VWF) was identified as a potential key target of NaB in the regulation of COPD. qRT-PCR and Western blot analysis showed that CSE significantly upregulated VWF expression in human umbilical vein endothelial cells (HUVECs), while NaB treatment markedly suppressed this upregulation. Using small interfering RNA (si-VWF), we knocked down VWF expression in HUVECs and co-cultured these cells with THP-1 cells in CSE-containing medium. ELISA, qRT-PCR, and Western blot analysis revealed that CSE enhanced the inflammatory response and activation of the PI3K-AKT signaling pathway in the THP-1. However, VWF knockdown reversed these effects of CSE. Furthermore, NaB pre-treatment of HUVECs significantly inhibited the inflammatory response and PI3K-AKT signaling activation in THP-1 cells, whereas VWF overexpression partially reversed the inhibitory effects of NaB. This study elucidated the critical regulatory role of VWF in CSE-induced endothelial cell-macrophage crosstalk and demonstrated that NaB suppresses CSE-induced VWF upregulation in HUVECs, thereby mitigating macrophage inflammation. Our findings reveal a novel mechanism by which NaB inhibits CSE-induced inflammation and highlight the therapeutic potential of NaB in COPD.
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