ArticleAnimal models and experimental medicine2026
Polydatin alleviates mitochondrial damage and apoptosis of lung epithelial cells by inhibiting toll-like receptor 4-dependent macrophage activation in asthma.
Article in Animal models and experimental medicine, 2026. 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.
- Resveratrol and the NLRP3 Inflammasome: Unlocking the Anti-inflammatory Potential of a Natural Compound.Current pharmaceutical design · 2026Review
- Polydatin alleviates mitochondrial damage and apoptosis of lung epithelial cells by inhibiting toll-like receptor 4-dependent macrophage activation in asthma.Animal models and experimental medicine · 2026Article
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10 authors.
Funding
Abstract
backgroundThis study investigated the role of polydatin in regulating macrophage-epithelial cell (EC) interactions during asthma. An asthma model was induced in BALB/c mice using ovalbumin (20 μg).
methodsThe therapeutic effects of polydatin (20 and 40 mg/kg) were evaluated in this asthmatic mouse model. To assess the underlying mechanisms, Bronchial Epithelium Adenovirus 12-SV40 2B (BEAS-2B) cells were cocultured with Tohoku Hospital for Pediatrics-1 (THP-1) macrophages, in which toll-like receptor 4 (TLR4) was either overexpressed or knocked down, and subsequently stimulated with lipopolysaccharide (LPS) and ATP. THP-1 cells underwent a 1-h pretreatment with polydatin (50 and 100 μmol/L), Class Lipid Inhibitor-095 (CLI-095, TLR4 inhibitor, 1 μg/mL), or A438079 (P2X7R antagonist, 10 μmol/L) prior to LPS/ATP challenge.
resultsFindings from Western blotting, enzyme-linked immunosorbent assay, flow cytometry, real-time polymerase chain reaction, and immunofluorescence assays demonstrated that modulating TLR4 expression significantly altered interleukin-1β (IL-1β) secretion from THP-1 macrophages and mitochondrial reactive oxygen species (mtROS) production in BEAS-2B ECs. In the mouse asthma model, polydatin significantly alleviated airway inflammation, oxidative stress, and apoptosis, likely by interfering with TLR4/P2X7R-mediated signaling and suppressing the activation of the NOD-like receptor protein inflammasome. Additionally, polydatin significantly reduced IL-1β and IL-18 levels and inhibited the infiltration of macrophages and eosinophils. Correspondingly, polydatin significantly attenuated TLR4/P2X7R signaling in THP-1 cells stimulated with ATP and LPS, thereby reducing IL-1β and IL-18 secretion, calcium influx, mtROS production, and apoptosis in BEAS-2B ECs.
conclusionsPolydatin is a promising therapeutic candidate for asthma, possibly by targeting macrophage-epithelium cross-talk via the TLR4/P2X7R axis. Future formulations as capsules or sprays may effectively alleviate airway inflammation and remodeling.
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