ArticleBiology direct2026
Rosavin alleviates COPD via inhibition of IL-17-enriched NET formation and NF-κB signaling.
Article in Biology direct, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundChronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide and is characterized by persistent inflammation, microbiota dysbiosis, and excessive neutrophil extracellular trap (NET) formation. Rosavin, a natural phenylpropanoid glycoside, exhibits anti-inflammatory and immunomodulatory activities, but its therapeutic potential in COPD remains unclear.
methodsA COPD rat model was induced by intratracheal lipopolysaccharide instillation combined with chronic passive cigarette smoke exposure. Rosavin (50 or 100 mg/kg) or the NF-κB inhibitor BAY 11-7082 (3 mg/kg) was administered for treatment. Pulmonary function tests (FEV1/FVC, PEF, and airway resistance), histopathological evaluation (HE and PAS staining), bronchoalveolar lavage fluid (BALF) inflammatory cell counts, ELISA-based cytokine assays, and oxidative stress markers (MDA, MPO, and SOD) were systematically assessed. NET formation was evaluated using MPO-DNA ELISA, Western blotting, and immunofluorescence for CitH3 and MPO/IL-17 colocalization. In addition, lung microbiota composition was analyzed by 16 S rRNA gene sequencing. Cigarette smoke extract (CSE)-stimulated BEAS-2B cells were used to assess the direct effects of Rosavin on NF-κB activation in vitro.
resultsRosavin significantly inhibited NF-κB activation, improved lung function, and reduced structural damage, oxidative stress, and inflammatory cytokines in COPD rats. It also suppressed NET formation, including IL-17-enriched NETs, by downregulating MPO, NE, and CitH3. In BEAS-2B cells, Rosavin similarly reduced CSE-induced NF-κB activation and cytokine release. Microbiota profiling showed decreased diversity and enrichment of Fusobacterium nucleatum in COPD rats, whereas Rosavin restored beneficial taxa such as Lactobacillus spp. BAY 11-7082 produced comparable effects, supporting NF-κB inhibition as a key mechanism.
conclusionRosavin ameliorates COPD-associated pathology through integrated mechanisms involving NF-κB inhibition, reduction of IL-17-enriched NET formation, and modulation of lung microbiota composition. These findings identify Rosavin as a promising multi-target therapeutic candidate for COPD.
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