Oligosaccharides from Polygonatum cyrtonema Hua ameliorate colitis-induced lung injury via inhibiting inflammation and oxidative stress

Lung disease is one of the parenteral manifestations of ulcerative colitis (UC), and still requires attention to the impact on the lungs while treating UC. Oligosaccharides from Polygonatum cyrtonema Hua (PFOS) has the therapeutic potential for lung injury associated with enteritis.To investigate the mechanism of PFOS in treating colitis-induced lung injury through NF-kB/Nrf2 signaling pathway, this study constructed in vitro and in vivo injury models using DSS and LPS. PFOS was used for the drug treatment, and Nrf2 inhibitor ML385 was used to interfere with Nrf2/HO-1 signaling pathway in the cells. In vivo results showed that PFOS reduces lung tissue damage associated with enteritis by protecting the epithelial barrier and regulating the Nrf2/NF-κB signaling pathways. PFOS upregulates antioxidant proteins (Nrf2, HO-1, NQO-1) and suppresses pro-inflammatory markers (p65, p-p65, IKK-β), indicating its antioxidant and anti-inflammatory effects. In vitro results showed that PFOS suppressed epithelial barrier damages, inflammation and oxidative stress in lung epithelial cells by inhibiting the NF-kB pathway and upregulating the Nrf2 signaling pathway. Additionally, PFOS intervention ameliorated the DSS-induced amino acid and lipid metabolism disorder.In conclusion,the DSS induced enteritis associated lung injury model, PFOS inhibited epithelial barrier damages, inflammation and oxidative stress of lung suppressed NF-kB and up regulated Nrf2 signaling pathway. Additionally, PFOS’s impact on intestinal metabolites may contribute to further protect lung tissue.