This study aimed to develop a submicron emulsion (SE) of Acer truncatum seed oil (ASO) and Rose roxburghii Tratt juice (RRTJ) using a response surface method for optimal formula screening and process parameters. The stability of ASO-RRTJ/SE and its effects on scopolamine-induced memory impairment in mice were investigated. The ASO-RRTJ/SE exhibited a desirable particle size ((276.86 ± 4.61) nm), polydispersity index (PDI, 0.22 ± 0.02), centrifugal stability parameter (Ke, 0.143 ± 0.004), and Zeta potential ((30.57 ± 2.38) mV). Morris water maze test, measurement of acetylcholine (ACh) concentration and acetylcholinesterase (AChE) activity in the hippocampus, superoxide dismutase (SOD) activity and malondialdehyde (MDA) concentration in serum, hematoxylin and eosin (H&E) staining, immunofluorescence staining were adopt to evaluate ASO-RRTJ/SE therapeutic potential in alleviating scopolamine-induced memory impairment in mice. Behavioral tests demonstrated that ASO-RRTJ/SE significantly ameliorated scopolamine-induced spatial learning and memory deficits in mice, suggesting potential neuroprotective effects against scopolamine-mediated central nervous system excitation. Compared to the Model group, the high-dose ASO-RRTJ/SE (H-SE) group displayed a 77.84% increase in hippocampal ACh content, a 46.97% decrease in AChE activity, a 29.48% increase in serum SOD activity, and a 40.15% decrease in MDA content. H&E staining of hippocampal sections revealed that the H-SE group exhibited well-organized hippocampal neurons, with a significantly reversal of nuclear pyknosis, deep staining, and cytoplasmic dissolution. The pyramidal cell layer displayed improved organization, and the intercellular distance returned to normal. Additionally, H-SE treatment significantly reduced the aggregation of phosphorylated tau protein, increased choline acetyltransferase expression, and promoted brain-derived neurotrophic factor production. In conclusion, ASO-RRTJ/SE ameliorates scopolamine-induced memory impairment in mice.

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.