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the same time, the metabolites were identified by searching database, and the main databases were the&amp;nbsp;HMDB (http://www.hmdb.ca/), Metlin ( https://metlin.scripps.edu/)&amp;nbsp;&amp;nbsp;.&amp;nbsp;&lt;/p></metabolite_identification_protocol><repository>MetaboLights</repository><study_status>Public</study_status><ptm_modification></ptm_modification><instrument_platform>Liquid Chromatography MS - positive - hilic</instrument_platform><instrument_platform>Liquid Chromatography MS - negative - hilic</instrument_platform><chromatography_protocol>&lt;p>Chromatographic separation was performed using a Thermo Ultimate 3000 ultrahigh-performance liquid chromatography system equipped with an ACQUITY UPLC HSS T3 column (2.1 × 100 mm, 1.8 μm). The flow rate was 0.3 mL/min, the column temperature was 40 °C, and the injection volume was 2 μL. In positive-ion mode, mobile phase A was water containing 0.1% formic acid and mobile phase B was acetonitrile containing 0.1% formic acid. In negative-ion mode, mobile phase C was 5 mmol/L aqueous ammonium formate and mobile phase D was acetonitrile. The same gradient was used in both ionization modes: 0–1 min, 10% organic phase; 1–7.5 min, 10–98%; 7.5–10 min, 98%; 10–10.1 min, 98–10%; and 10.1–12 min, 10%.&lt;/p></chromatography_protocol><publication>Schisandra chinensis alleviates dextran sulfate sodium-induced colitis in association with remodeling of a Parabacteroides goldsteinii-related leucine– isovalerate metabolic axis and attenuation of mTOR/HIF-1α/IL-17 signaling.</publication><submitter_affiliation>nanjing university of chinese medicine</submitter_affiliation><submitter_name>Jiuba Zhang</submitter_name><organism_part>feces</organism_part><technology_type>mass spectrometry assay</technology_type><disease></disease><extraction_protocol>&lt;p>Fecal samples (50 mg) were extracted with 600 μL of methanol–water (4:1, v/v) containing 2-chloro-L-phenylalanine as an internal standard. Samples were homogenized at 60 Hz for 120 s at 4 °C and then sonicated in an ice bath for 10 min. After centrifugation at 12000 × g&amp;nbsp;for 10 min at 4 °C, the supernatants were passed through 0.22-μm membrane filters for LC–MS analysis. Equal aliquots from all samples were pooled to prepare quality&amp;nbsp;control&amp;nbsp;samples.&lt;/p></extraction_protocol><organism>Mus musculus</organism><full_dataset_link>https://www.ebi.ac.uk/metabolights/MTBLS15496</full_dataset_link><author>Jiuba Zhang. nanjing university of chinese medicine. zhang15895865293@163.com.</author><data_transformation_protocol>&lt;p>The pretreatment of LC/MS raw data was performed by&amp;nbsp;Progenesis QI (Waters Corporation, Milford, USA)&amp;nbsp;software, and a three-dimensional data matrix in CSV format was exported. The information in this three-dimensional matrix included: sample information, metabolite name and mass spectral response intensity. Internal standard peaks, as well as any known false positive peaks (including noise, column bleed, and derivatized reagent peaks), were removed from the data matrix, deredundant and peak pooled.&lt;/p></data_transformation_protocol><study_factor>Treatment</study_factor><submitter_email>zhang15895865293@163.com</submitter_email><sample_collection_protocol>&lt;p>Fresh mouse fecal samples were collected immediately after defecation, rapidly transferred into sterile cryotubes, and promptly immersed in liquid nitrogen for snap-freezing. The frozen samples were then stored in liquid nitrogen until further processing to preserve microbial composition and metabolic integrity for subsequent analyses.&lt;/p></sample_collection_protocol><omics_type>Metabolomics</omics_type><study_design>Metabolomics</study_design><study_design>Mus musculus</study_design><study_design>untargeted analysis</study_design><study_design>Parabacteroides goldsteinii</study_design><study_design>mTOR/HIF-1α/IL-17 signaling</study_design><study_design>Ulcerative</study_design><study_design>Thermo Scientific Dionex Ultimate 3000 HPLC system</study_design><study_design>leucine–isovalerate axis</study_design><study_design>Schisandra chinensis</study_design><study_design>Thermo Scientific Q Exactive</study_design><study_design>ulcerative colitis</study_design><study_design>experimental blank</study_design><study_design>feces</study_design><curator_keywords>Metabolomics</curator_keywords><curator_keywords>Mus musculus</curator_keywords><curator_keywords>untargeted analysis</curator_keywords><curator_keywords>Parabacteroides goldsteinii</curator_keywords><curator_keywords>mTOR/HIF-1α/IL-17 signaling</curator_keywords><curator_keywords>Ulcerative</curator_keywords><curator_keywords>Thermo Scientific Dionex Ultimate 3000 HPLC system</curator_keywords><curator_keywords>leucine–isovalerate axis</curator_keywords><curator_keywords>Schisandra chinensis</curator_keywords><curator_keywords>Thermo Scientific Q Exactive</curator_keywords><curator_keywords>experimental blank</curator_keywords><curator_keywords>ulcerative colitis</curator_keywords><curator_keywords>feces</curator_keywords><mass_spectrometry_protocol>&lt;p>Mass spectrometry was performed on a Thermo Q Exactive high-resolution mass spectrometer equipped with an electrospray ionization source. Data were acquired in both positive- and negative-ion modes. The spray voltages were 3.50 and −2.50 kV, respectively. The sheath gas and auxiliary gas were set to 40 and 10 arbitrary units, and the capillary temperature was 325 °C. Full-scan spectra were acquired over m/z 81–1000 at a resolution of 70000. Tandem mass spectra were acquired by higher-energy collisional dissociation at 30 eV and a resolution of 17,500.&lt;/p></mass_spectrometry_protocol><metabolite_name>ST 21_2;O5</metabolite_name><metabolite_name>Phosphatidylethanolamine lyso alkenyl 16</metabolite_name><metabolite_name>LysoPE(0_0_18_2(9Z,12Z))</metabolite_name><metabolite_name>(2Z)-4,6-dihydroxy-2-[(4-hydroxy-3,5-dimethoxyphenyl)methylidene]-1-benzofuran-3-one</metabolite_name><metabolite_name>Propyl 4-(3-bromo-4-methoxyphenyl)-2,7,7-trimethyl-5-oxo-1,4,5,6,7,8-hexahydroquinoline-3-carboxylate</metabolite_name><metabolite_name>Avermectin A1b aglycone</metabolite_name><metabolite_name>Glu-Thr</metabolite_name><metabolite_name>[(3S,4S,5S,6R)-3,4,5,6-tetrahydroxycyclohexen-1-yl]methyl dihydrogen phosphate</metabolite_name><metabolite_name>4,4-Thiodianiline</metabolite_name><metabolite_name>8-Aminooctanoic acid</metabolite_name><metabolite_name>Quillaic Acid</metabolite_name><metabolite_name>N-Acetyl-L-tyrosine</metabolite_name><metabolite_name>Rotenolone</metabolite_name><metabolite_name>Ethyl Dodecanoate</metabolite_name><metabolite_name>LysoPE(14_0_0_0)</metabolite_name><metabolite_name>Fluorouracil</metabolite_name><metabolite_name>Spiradine A</metabolite_name><metabolite_name>1,1-Dimethyl-2,7-dibromo-4a-(bromomethyl)-1,2,3,4,4a,9a-hexahydro-9H-xanthene</metabolite_name><metabolite_name>Calcitroic acid</metabolite_name><metabolite_name>13-Desoxyterpendole I</metabolite_name><metabolite_name>L-2-Amino-4-methylenepentanedioic acid</metabolite_name><metabolite_name>Geranylfarnesyl diphosphate</metabolite_name><metabolite_name>Chrysin</metabolite_name><metabolite_name>Premithramycin A2</metabolite_name><metabolite_name>6-[3-methoxy-4-(naphthalen-1-ylmethoxy)phenyl]-9,9-dimethyl-6,8,10,11-tetrahydro-5H-benzo[b][1,4]benzodiazepin-7-one</metabolite_name></additional><is_claimable>false</is_claimable><name>Schisandra chinensis alleviates dextran sulfate sodium-induced colitis in association with remodeling of a Parabacteroides goldsteinii-related leucine– isovalerate metabolic axis and attenuation of mTOR/HIF-1α/IL-17 signaling</name><description>&lt;p>Ulcerative colitis (UC) involves epithelial injury, gut microbial dysbiosis, disturbed microbial metabolism, and mucosal inflammation. This study evaluated the protective effect of Schisandra chinensis (SC) against dextran sulfate sodium (DSS)-induced UC and investigated the underlying microbiota–metabolite–host signaling mechanism. UPLC-Q-TOF-MS/MS identified 38 constituents in SC, predominantly lignans, organic and phenolic acids, and terpenoids. SC reduced body weight loss, disease activity, colon shortening, mucosal and histological injury, and pro-inflammatory cytokine levels, while partially restoring claudin-1 and occludin expression. Metagenomic analysis showed that SC restructured the DSS-disrupted microbiota, enriched Parabacteroides goldsteinii, and increased the predicted abundance of pathways related to valine, leucine, and isoleucine degradation. Untargeted metabolomics and targeted fatty acid analysis showed lower fecal leucine and higher isovalerate levels after SC treatment. Whole-colon transcriptomic and western blot analyses further demonstrated that SC suppressed the mTOR/HIF-1α/STAT3/IL-17 inflammatory program in colonic tissue. Antibiotic pretreatment weakened several protective effects of SC, whereas P. goldsteinii or sodium isovalerate administration partially recapitulated its anti-inflammatory and barrier-restorative effects. Conversely, the mTOR activator MHY1485 attenuated SC-mediated protection. These findings indicate that the protective effects of SC are associated with remodeling of a P. goldsteinii-related leucine–isovalerate metabolic network and attenuation of colonic mTOR/HIF-1α/STAT3/IL-17 signaling. This study provides a microbiota-centered mechanistic basis for the therapeutic potential of SC in UC.&lt;/p></description><dates><publication>2026-08-29</publication><submission>2026-08-29</submission></dates><accession>MTBLS15496</accession><cross_references/></HashMap>