Xiuli Gao

Background: Qijiao Shengbai capsule (QJSB) is a classic traditional Chinese compound formulation composed of seven herbal ingredients, primarily used clinically to treat leukopenia. Individual herbs and their active components within QJSB demonstrate favorable efficacy against ulcerative colitis (UC). Nevertheless, no evidence exists of QJSB being a full-form prescription for treating UC. Methods: This study identified the chemical composition of QJSB using UHPLC-ESI-Q-Exactive Plus Orbitrap-MS. At the same time, a mouse model of ulcerative colitis (UC) was established using DSS to examine the effects of QJSB on disease symptoms, inflammatory factors, intestinal barrier function, and colonic histopathological changes. Furthermore, metabolomics, 16S rRNA sequencing, and network pharmacology were combined to analyze the potential mechanisms underlying the effects of QJSB intervention in UC-affected mice, and key pathways predicted by network pharmacology were validated using Western blot analysis. Results: The results showed that QJSB treatment significantly alleviated DSS-induced colitis symptoms in UC mice, as evidenced by weight recovery, a decrease in the disease activity index (DAI), improvement in colonic shortening, and reduced tissue damage. Gut microbiota analysis indicated that QJSB modulates the composition of the gut microbiota by upregulating the abundance of Akkermansia and Lactobacillus and downregulating the abundance of Bacteroides . Metabolomics results suggest that QJSB may help correct metabolic disturbances involving amino acids, linoleic acid, arachidonic acid, and alpha-linolenic acid. Furthermore, QJSB was associated with reduced levels of pro-inflammatory factors (TNF-α, IL-6, IL-1β), lipopolysaccharide (LPS), and myeloperoxidase (MPO), as well as improved intestinal barrier function. Western blot results suggest that QJSB intervention may be associated with the suppression of TLR4/MyD88/NF-κB signaling pathway activation. Conclusion: The present findings suggest that QJSB may exert therapeutic effects against UC, potentially through mechanisms involving the inhibition of inflammatory responses, protection of intestinal barrier function, regulation of metabolic homeostasis, and restoration of gut microbial ecology. These results imply that QJSB could serve as a potential therapeutic candidate for UC and provide a new basis for its clinical application.

Background: Diarrhea-predominant irritable bowel syndrome (IBS-D) is a common functional bowel disorder closely associated with gut microbiota dysbiosis and gut-brain axis dysfunction. However, effective treatment options remain limited. In this study, we investigated the therapeutic effects and underlying mechanisms of an extract derived from the pulp of Rosa roxburghii Tratt after co-fermentation with Saccharomyces cerevisiae and Bacillus subtilis (referred to as FRRTP) in a mouse model of IBS-D. Methods: Rosa roxburghii Tratt pulp Co-fermented with Saccharomyces cerevisiae and Bacillus subtilis , followed by extraction, was analyzed by UPLC-Q-Exactive Orbitrap-rbitrap OrExactive Oron, was ouse model of IBS-D. This study, we investigated the therapeutic effects and underlying mechanisms of an extract derived from the pulp of t version, please let us know that does nointragastric Senna Folium extract. After FRRTP intervention, diarrhea symptoms, abdominal withdrawal reflex, behavioral tests, colon and brain histopathology, inflammatory cytokines, and gut-brain neurotransmitters were evaluated. Gut microbiota was analyzed by 16S rRNA sequencing. Untargeted metabolomics was performed on serum and colon samples, and AFADESI-MSI spatial metabolomics was used to map metabolic alterations in the brain. Results: Co-fermentation significantly increased the variety and content of bioactive components (e.g., flavonoids and polyphenols) in Rosa roxburghii Tratt pulp. Compared with the model group, FRRTP alleviated diarrhea, visceral hypersensitivity, colonic damage, and brain histopathological damage, reduced TNF-α, IL-6, and IL-1β levels; modulated brain-gut neuropeptides (5-HT, SP, VIP); and improved anxiety-like behaviors. 16S rRNA sequencing revealed that FRRTP reversed gut microbiota dysbiosis by increasing beneficial bacteria and reducing the proportion of pathogenic bacteria. Metabolomics showed that FRRTP regulated tryptophan, purine, and glycerophospholipid pathways, spatial metabolomics confirmed that FRRTP ameliorated the disturbed cerebral distribution of 5-HT, tryptophan, glycerophosphocholine, dopamine, and adrenaline. Conclusion: Our findings demonstrate that FRRTP alleviates IBS-D symptoms in mice by modulating the gut microbiota and correcting metabolic disturbances, supporting its potential development as a functional food or therapeutic agent for IBS-D.

Depression is a common mental disorder that substantially impairs patients’ daily life and work. To identify natural and safe preventive options, we investigated the preventive effect and underlying mechanism of the Ganoderma lucidum and Rosa roxburghii Tratt formula (GLRRTF) on depression. A total of 72 chemical components in GLRRTF were identified by UHPLC-ESI-Q-Exactive Plus Orbitrap-MS Analysis. GLRRTF (containing 400 mg/kg of G. lucidum extract and 800 mg/kg of R. roxburghii extract per day), administered as a 1-week preventive intervention followed by 4 weeks of co-administration with chronic unpredictable mild stress, prevented the development of depression-like behaviors in male C57BL/6J mice and reduced neuronal damage in the hippocampus. Airflow-assisted desorption electrospray ionization mass spectrometry imaging and enzyme-linked immunosorbent assays showed that GLRRTF corrected abnormalities in neurotransmitter levels. The 16S rRNA sequencing indicated that GLRRTF restored dysbiosis of the gut microbiota. Metabolomic profiling revealed that GLRRTF increased the level of tryptophan and promoted tryptophan metabolism towards the 5-HT and indole pathways in feces and the brain. Western blot demonstrated that GLRRTF increased 5-HT production from tryptophan in the brain by regulating tryptophan hydroxylase 2 and DOPA decarboxylase. GLRRTF activated the PI3K/AKT pathway by regulating brain-derived neurotrophic factor and its receptor tropomyosin receptor kinase B. This research provides a comprehensive mechanistic understanding of GLRRTF’s preventive effect against depression, highlighting its potential as a novel, safe, and preventive functional food formulation.

FeMn dual-active-site single-atom catalyst (FeMn-N–C), featuring manganese-enhanced Fe–N-doped carbon with abundant FeMn-N4 and C-N active groups, was fabricated via hydrothermal synthesis followed by high-temperature pyrolysis. Thiocyanate (SCN⁻) can be adsorbed onto the FeMn–N–C surface by binding to Fe/Mn atoms, blocking the active sites of the mimic peroxidase and thereby inhibiting the corresponding chromogenic reaction of 3,3’,5,5’-tetramethylbenzidine, achieving rapid and sensitive colorimetric detection of SCN⁻. Under optimal conditions, the established biosensor exhibited a linear range of 0.2–11 μmol L⁻¹, with a detection limit of 66.7 nmol L⁻¹. Experimental findings and theoretical calculations demonstrated that the superior activity of FeMn–N–C stemmed from the synergistic effect of the dual atoms, which boosted substrate adsorption and reduced the reaction barrier. This strategy provided mechanistic insights into the rational design of advanced nanozymes, highlighting their potential for food safety and environmental monitoring applications. Graphical Abstract