Oligosaccharides from Polygonatum cyrtonema Hua ameliorate colitis-induced lung injury via modulation of the gut-lung axis through NF-κB and Nrf2 pathways

doi:10.1007/s13659-026-00608-0

Natural Products and Bioprospecting ›› 2026, Vol. 16 ›› Issue (5): 70-70.DOI: 10.1007/s13659-026-00608-0

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Oligosaccharides from Polygonatum cyrtonema Hua ameliorate colitis-induced lung injury via modulation of the gut-lung axis through NF-κB and Nrf2 pathways

Jin Xu¹, Chuankang Tang², Qianyu He³, Yu Lu³, Pei Luo^4,5, Jianbo Wu³

1. Department of Science and Technology, Department of Gastroenterology, Luzhou People's Hospital, Luzhou, 646000, China;
2. Department of Gastroenterology, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China;
3. Basic Medicine Research Innovation Center for Cardiometabolic Diseases, Ministry of Education, Laboratory for Cardiovascular Pharmacology, Department of Pharmacology, School of Pharmacy, Luzhou Municipal Key Laboratory of Thrombosis and Vascular Biology, Southwest Medical University, Luzhou, 646000, China;
4. Faculty of Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Macau, People's Republic of China;
5. State Key Laboratory of Quality Research in Chinese Medicine (Macau University of Science and Technology), Avenida Wai Long, Macau, People's Republic of China

Received:2025-11-27 Accepted:2026-02-10 Online:2026-10-08
Supported by:
This work was supported by Sichuan Province Science and Technology Agency Grant (2024NSFSC0591),Luzhou-Southwest Medical University’s scientific research project (2018-ZRQN-159),Medical Research Projects and Youth Innovation Projects of Sichuan Medical Association (Q20250041),and Luzhou-Southwest Medical University Cooperation Project (23YKDCXY0003).

Oligosaccharides from Polygonatum cyrtonema Hua ameliorate colitis-induced lung injury via modulation of the gut-lung axis through NF-κB and Nrf2 pathways

Jin Xu¹, Chuankang Tang², Qianyu He³, Yu Lu³, Pei Luo^4,5, Jianbo Wu³

1. Department of Science and Technology, Department of Gastroenterology, Luzhou People's Hospital, Luzhou, 646000, China;
2. Department of Gastroenterology, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China;
3. Basic Medicine Research Innovation Center for Cardiometabolic Diseases, Ministry of Education, Laboratory for Cardiovascular Pharmacology, Department of Pharmacology, School of Pharmacy, Luzhou Municipal Key Laboratory of Thrombosis and Vascular Biology, Southwest Medical University, Luzhou, 646000, China;
4. Faculty of Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Macau, People's Republic of China;
5. State Key Laboratory of Quality Research in Chinese Medicine (Macau University of Science and Technology), Avenida Wai Long, Macau, People's Republic of China

通讯作者: Jin Xu,E-mail:760291440@qq.com;Pei Luo,E-mail:pluo@must.edu.mo;Jianbo Wu,E-mail:jbwucn@163.com
基金资助:
This work was supported by Sichuan Province Science and Technology Agency Grant (2024NSFSC0591),Luzhou-Southwest Medical University’s scientific research project (2018-ZRQN-159),Medical Research Projects and Youth Innovation Projects of Sichuan Medical Association (Q20250041),and Luzhou-Southwest Medical University Cooperation Project (23YKDCXY0003).

Abstract

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.

Key words: PFOS, Colitis-induced lung injury, NF-κB/IKK-β, Nrf2/HO-1/NQO-1, Mucosal barrier, Intestinal metabolites

摘要： Background The 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 methods Dextran 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.
Results PFOS 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.
Conclusions PFOS 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.

关键词: PFOS, Colitis-induced lung injury, NF-κB/IKK-β, Nrf2/HO-1/NQO-1, Mucosal barrier, Intestinal metabolites

Jin Xu, Chuankang Tang, Qianyu He, Yu Lu, Pei Luo, Jianbo Wu. Oligosaccharides from Polygonatum cyrtonema Hua ameliorate colitis-induced lung injury via modulation of the gut-lung axis through NF-κB and Nrf2 pathways[J]. Natural Products and Bioprospecting, 2026, 16(5): 70-70.

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Oligosaccharides from Polygonatum cyrtonema Hua ameliorate colitis-induced lung injury via modulation of the gut-lung axis through NF-κB and Nrf2 pathways

Oligosaccharides from Polygonatum cyrtonema Hua ameliorate colitis-induced lung injury via modulation of the gut-lung axis through NF-κB and Nrf2 pathways

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