ArticleNatural products and bioprospecting2026
Oligosaccharides from Polygonatum cyrtonema Hua ameliorate colitis-induced lung injury via modulation of the gut-lung axis through NF-κB and Nrf2 pathways.
Article in Natural products and bioprospecting, 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
backgroundThe gut-lung axis is a bidirectional communication network linking intestinal and pulmonary homeostasis through shared immunological and molecular mechanisms, conceptually consistent with the traditional Chinese medicine theory of "lung-intestine combined treatment." Polygonatum cyrtonema Hua is an edible medicinal plant with reported anti-inflammatory and antioxidant properties, yet its role in intestinal inflammation-associated lung injury remains unclear. MATERIALS AND
methodsDextran sulfate sodium (DSS)-induced colitis and lipopolysaccharide (LPS)-induced lung injury models were established in vivo, while LPS-stimulated A549 lung epithelial cells were used in vitro. The protective effects of Polygonatum cyrtonema oligosaccharides (PFOS) were evaluated, with particular focus on NF-κB and Nrf2 signaling pathways. The Nrf2 inhibitor ML385 was applied in vitro to verify pathway involvement. Non-targeted fecal metabolomics was conducted to assess PFOS-mediated metabolic modulation.
resultsPFOS significantly alleviated DSS-associated lung histopathological damage, reduced inflammatory cell infiltration, and improved epithelial barrier integrity. PFOS suppressed pulmonary proinflammatory cytokines, including TNF-α and IL-6, decreased myeloperoxidase activity, and attenuated oxidative stress by lowering malondialdehyde levels while enhancing antioxidant enzymes such as superoxide dismutase and HO-1. Mechanistically, PFOS inhibited NF-κB activation and promoted Nrf2/HO-1 signaling in lung tissues and LPS-stimulated A549 cells, effects that were partially reversed by ML385. Metabolomics analysis revealed that PFOS corrected DSS-induced disturbances in amino acid and lipid metabolism, with enrichment in cAMP, PPAR, and tryptophan-related pathways.
conclusionsPFOS protects against colitis-associated lung injury by modulating the gut-lung axis through coordinated anti-inflammatory and antioxidant mechanisms involving NF-κB inhibition and Nrf2 activation, supporting its potential therapeutic application in gut-lung axis-related diseases.
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