<HashMap><database>biostudies-literature</database><scores/><additional><submitter>He X</submitter><funding>National High Level Hospital Clinical Research Funding (Scientific and Technological Achievements Transformation Incubation Guidance Fund Project of Peking University First Hospital)</funding><funding>Beijing Nova Program</funding><funding>the National Natural Science Foundation of China</funding><funding>Peking University Clinical Scientist Training Program</funding><pagination>17673</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12095773</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(1)</volume><pubmed_abstract>Patients with ulcerative colitis (UC) have a significantly impaired intestinal barrier. Hydrogen Sulfide (H&lt;sub>2&lt;/sub>S) is a gaseous mediator that makes notable contributions in a variety of diseases, such as reducing inflammatory response in colitis. The experimental content includes the establishment of a mouse DSS-induced colitis mouse model, mouse colon epithelial organoids culture, H&amp;E staining and mass spectrometry analysis. We recognized that exogenous H&lt;sub>2&lt;/sub>S donor-GYY4137 significantly alleviated the symptoms in UC mice models and maintained Minichromosome Maintenance Complex Component 2 (MCM2) expression. CBS knockdown reduced the expression of sulfhydrated Ribosomal protein S20 (RPS20-ssh) and MCM2 in the mouse colon. Cell experiments indicated that the expression of RP</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Hydrogen sulfide preserves intestinal barrier repair function through sulfhydration of RPS20 in experimental colitis.</pubmed_title><pmcid>PMC12095773</pmcid><funding_grant_id>BMU2023PYJH001</funding_grant_id><funding_grant_id>32370837</funding_grant_id><funding_grant_id>20230484244</funding_grant_id><funding_grant_id>2023CX04</funding_grant_id><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Wang P</pubmed_authors><pubmed_authors>Xue B</pubmed_authors><pubmed_authors>Zhu J</pubmed_authors><pubmed_authors>Huang Z</pubmed_authors><pubmed_authors>You M</pubmed_authors><pubmed_authors>He X</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Chen S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Hydrogen sulfide preserves intestinal barrier repair function through sulfhydration of RPS20 in experimental colitis.</name><description>Patients with ulcerative colitis (UC) have a significantly impaired intestinal barrier. Hydrogen Sulfide (H&lt;sub>2&lt;/sub>S) is a gaseous mediator that makes notable contributions in a variety of diseases, such as reducing inflammatory response in colitis. The experimental content includes the establishment of a mouse DSS-induced colitis mouse model, mouse colon epithelial organoids culture, H&amp;E staining and mass spectrometry analysis. We recognized that exogenous H&lt;sub>2&lt;/sub>S donor-GYY4137 significantly alleviated the symptoms in UC mice models and maintained Minichromosome Maintenance Complex Component 2 (MCM2) expression. CBS knockdown reduced the expression of sulfhydrated Ribosomal protein S20 (RPS20-ssh) and MCM2 in the mouse colon. Cell experiments indicated that the expression of RP</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 May</publication><modification>2026-06-03T02:42:50.5Z</modification><creation>2026-04-23T03:11:37.154Z</creation></dates><accession>S-EPMC12095773</accession><cross_references><pubmed>40399407</pubmed><doi>10.1038/s41598-025-02268-5</doi></cross_references></HashMap>