@article{Pan2026, 
author = {Chengfeng Pan and Mei Peng and Keling Yang and Yu Wang and Lilang Li and Faju Chen and Qiji Li and Xiaosheng Yang and Liangqun Li and Juan Yang},
title = {Phallus impudicus polysaccharide protects against acute lung injury via inhibition of inflammatory/antioxidant pathways and regulation of gut microbiota and lung tissue metabolites},
year = {2026},
journal = {Food Science and Human Wellness},
keywords = {Phallus impudicus polysaccharide, acute lung injury, MAPK/NF-κB signalling pathway, Nrf2/Keap1/HO-1 signalling pathway, gut microbiota, metabolomics},
url = {https://www.sciopen.com/article/10.26599/FSHW.2026.9251016},
doi = {10.26599/FSHW.2026.9251016},
abstract = {Phallus impudicus L. (P. impudicus L.) is an edible fungus with a delicious taste and considerable medicinal-edible value. Preliminary studies have confirmed that its refined polysaccharide (PIRP) exhibit significant anti-inflammatory and antioxidant effects. Acute lung injury (ALI) is a severe disease characterized by severe inflammation and oxidative stress, with high incidence and mortality, yet lacks effective clinical treatments. This study aimed to evaluate protective effect of PIRP  against lipopolysaccharide-induced ALI in mice and comprehensively clarify its therapeutic mechanisms. The therapeutic efficacy of PIRP was assessed by testing the degree of pulmonary edema, antioxidant enzymes/peroxidases and inflammatory factors, as well as by histopathological analysis of the lungs. Furthermore, we investigated the mechanism of PIRP action using immunofluorescence, protein immunoblotting, transmission electron microscopy, 16S-rRNA gene sequencing, and metabolomics experiments. The results showed that PIRP significantly ameliorated histopathological lung damage in ALI mice, reduced bronchoalveolar lavage fluid (BALF) protein concentrations and inflammatory cytokine levels, and increased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). PIRP also improved mitochondrial structural integrity and effectively mitigated reactive oxygen species (ROS) accumulation caused by mitochondrial damage. Mechanistically, PIRP suppressed the expression of downstream proteins in the MAPK and NF-κB signaling pathways, thereby inhibiting the production of inflammatory factors and alleviating inflammation. Additionally, PIRP upregulated the expression of Nrf2 and HO-1 and downregulated Keap1 expression, stimulating antioxidant enzyme activity and ultimately mitigating LPS-induced oxidative stress imbalance. Furthermore, PIRP modulated the composition and structure of intestinal flora, decreasing the abundance of harmful bacteria while increasing beneficial bacterial genera, thereby ameliorating intestinal flora dysbiosis in ALI mice. Metabolomic analysis identified differentially abundant metabolites between LPS- and PIRP-treated groups; PIRP reversed LPS-induced dysregulation of 4-hydroxybutanoic acid, (R)-3-hydroxybutanoic acid, and L-aspartic acid. These findings demonstrate the multifaceted protective effects of PIRP against ALI and contribute to a deeper understanding of its anti-inflammatory, antioxidant, and microbiome-modulating functions.}
}