Re-Du-Ning Alleviates Airway-Intestinal Inflammation of COPD Rats by Regulating Glycerophospholipid Metabolism and Modulating Gut Microbiome.

RDN partially improved lung-function impairment and attenuated lung and colon histopathological changes in COPD rats.

• COPD was modeled in rats by combining cigarette smoke exposure with intratracheal LPS instillation.
• RDN was given intragastrically at gradient doses to assess in vivo efficacy.
• The abstract describes the improvement as partial, covering both airway (lung) and intestinal (colon) pathology.

RDN reduced IL-1β, TNF-α and IL-6 levels in serum, BALF and feces of COPD rats.

• Cytokine reductions were measured across three compartments: serum, bronchoalveolar lavage fluid (BALF), and feces.
• This supports an anti-inflammatory effect spanning both the airway and the gut.

RDN partially restored glycerophospholipid metabolic profiles in COPD rats.

• Untargeted metabolomics was used to screen differential metabolites after RDN intervention.
• KEGG enrichment analysis identified glycerophospholipid metabolism as a core pathway.
• The restoration was described as partial.

RDN reshaped gut microbiota composition in COPD rats, and a 'host phenotype-metabolite-gut microbiota' network was constructed.

• 16S rRNA sequencing was used to identify differential gut bacterial genera after RDN intervention.
• Correlation analysis linked host phenotypes, metabolites and gut bacteria into a network.

An intact gut microbiota was required for the full protective effect of RDN, and part of the effect was transferable by FMT.

• Antibiotic-mediated gut microbiota depletion was used to test whether the microbiota is needed for RDN's effect.
• Fecal microbiota transplantation (FMT) experiments suggested that part of RDN's protective effect can be transferred.

LPC (14:0) and LPC (16:0) regulated cytokine release in BEAS-2B cells.

• Targeted glycerophospholipid supplementation was used for functional validation.
• BEAS-2B cells are a human bronchial epithelial cell line.

Data from a human GEO cohort further validated a role for glycerophospholipid metabolism in COPD.

• Human clinical cohort datasets from the Gene Expression Omnibus (GEO) were used for validation.
• This supports the relevance of the rat findings to human COPD.