<HashMap><database>MetaboLights</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Tabular>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS14222/m_MTBLS14222_LC-MS_positive_reverse-phase_v2_maf.tsv</Tabular><Tabular>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS14222/m_MTBLS14222_LC-MS_negative_reverse-phase_v2_maf.tsv</Tabular><Txt>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS14222/i_Investigation.txt</Txt><Txt>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS14222/s_MTBLS14222.txt</Txt><Txt>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS14222/a_MTBLS14222_LC-MS_negative_reverse-phase.txt</Txt><Txt>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS14222/a_MTBLS14222_LC-MS_positive_reverse-phase.txt</Txt></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><ftp_download_link>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS14222</ftp_download_link><metabolite_identification_protocol>&lt;p>OmicStudio tool (https://www.omicstudio.cn/tool)&lt;/p></metabolite_identification_protocol><repository>MetaboLights</repository><study_status>Public</study_status><ptm_modification></ptm_modification><instrument_platform>Liquid Chromatography MS - negative - reverse-phase</instrument_platform><instrument_platform>Liquid Chromatography MS - positive - reverse-phase</instrument_platform><chromatography_protocol>&lt;p>Serum metabolites were extracted with 80% methanol on ice and analyzed using an LC-MS system comprised of an UltiMate 3000 UPLC coupled to an ACQUITY UPLC T3 column (100mm×2.1mm, 1.8μm; Waters) maintained at 40.&lt;/p></chromatography_protocol><publication>Microbial tryptophan metabolism orchestrated by trilobatin through TPH1 activation protects against acute kidney injury.</publication><submitter_affiliation>Zunyi medical university</submitter_affiliation><submitter_name>jiajia wei</submitter_name><organism_part>Blood</organism_part><technology_type>mass spectrometry assay</technology_type><disease></disease><extraction_protocol>&lt;p>The mobile phase consisted of 5 mM ammonium acetate with 5mM acetic acid (solvent A) and acetonitrile (solvent B), and was eluted at a flow rate of 0.3 ml/min using a gradient program in which solvent B was maintained at 2% from 0 to 0.8 min, increased from 2% to 70% between 0.8 and 2.8 min, further raised to 90% by 5.6 min, then to 100% by 6.4 min, held at 100% until 8.0 min, rapidly decreased to 2% at 8.1 min, and finally held at 2% until 10 min.&lt;/p></extraction_protocol><organism>Homo sapiens</organism><full_dataset_link>https://www.ebi.ac.uk/metabolights/MTBLS14222</full_dataset_link><author>Jianmei Gao. Zunyi medical university. gaojianmei@zmu.edu.cn.</author><author>Jiajia Wei. Zunyi medical university. 1610059073@qq.com.</author><data_transformation_protocol>&lt;p>OmicStudio tool (https://www.omicstudio.cn/tool)&lt;/p></data_transformation_protocol><study_factor>Group</study_factor><submitter_email>1610059073@qq.com</submitter_email><sample_collection_protocol>&lt;p>Mice were then anesthetized, and blood samples were collected from the retro-orbital plexus. Serum was separated, with 100 μL allocated for metabolomic profiling and the remainder stored at -80 °C for subsequent experiments.&lt;/p></sample_collection_protocol><omics_type>Metabolomics</omics_type><study_design>Metabolomics</study_design><study_design>Microbiota-gut-kidney axis</study_design><study_design>Serotonin</study_design><study_design>Tryptophan metabolism</study_design><study_design>untargeted analysis</study_design><study_design>Acute kidney injury</study_design><study_design>Thermo Scientific Vanquish Flex UHPLC System</study_design><study_design>Thermo Scientific Orbitrap Exploris 120</study_design><study_design>Trilobatin</study_design><study_design>Homo sapiens</study_design><study_design>Serum</study_design><study_design>Blood</study_design><curator_keywords>Metabolomics</curator_keywords><curator_keywords>Serotonin</curator_keywords><curator_keywords>Microbiota-gut-kidney axis</curator_keywords><curator_keywords>Tryptophan metabolism</curator_keywords><curator_keywords>untargeted analysis</curator_keywords><curator_keywords>Thermo Scientific Vanquish Flex UHPLC System</curator_keywords><curator_keywords>Thermo Scientific Orbitrap Exploris 120</curator_keywords><curator_keywords>Acute kidney injury</curator_keywords><curator_keywords>Trilobatin</curator_keywords><curator_keywords>Serum</curator_keywords><curator_keywords>Homo sapiens</curator_keywords><curator_keywords>Blood</curator_keywords><mass_spectrometry_protocol>&lt;p>Mass spectrometry data were acquired in both positive and negative ion modes with full MS scans at 70,000 resolution.&lt;/p></mass_spectrometry_protocol></additional><is_claimable>false</is_claimable><name>Microbial tryptophan metabolism orchestrated by trilobatin through TPH1 activation protects against acute kidney injury</name><description>Background: Acute kidney injury (AKI) remains a major clinical challenge with limited therapeutic options. Gut microbiota dysbiosis plays a crucial role in the pathogenesis of AKI. Trilobatin (TLB), has been previously reported to modulate gut microbiota and exert neuroprotective effects; however, its potential role in renal protection remains unknown. Results: In this study, we demonstrate that TLB treatment significantly alleviates renal dysfunction and pathological damage in an AKI mouse model. Moreover, TLB restored intestinal barrier integrity by upregulating key tight junction proteins. 16S rRNA sequencing revealed that TLB modulated the gut microbiota composition, notably enriching Lachnospiraceae, which facilitated tryptophan metabolism and elevated serotonin production. Mechanistically, tryptophan hydroxylase 1 (TPH1) was identified as a direct target of TLB. Conclusions: Our findings unveil a previously unrecognized role of TLB in ameliorating AKI through microbiota-gut-kidney axis regulation, highlighting the therapeutic potential of microbial and metabolic intervention in AKI</description><dates><publication>2026-04-05</publication><submission>2026-04-05</submission></dates><accession>MTBLS14222</accession><cross_references/></HashMap>