<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>43(7)</volume><submitter>Li TT</submitter><pubmed_abstract>We previously show that L-Cysteine administration significantly suppresses hypoxia-ischemia (HI)-induced neuroinflammation in neonatal mice through releasing H&lt;sub>2&lt;/sub>S. In this study we conducted proteomics analysis to explore the potential biomarkers or molecular therapeutic targets associated with anti-inflammatory effect of L-Cysteine in neonatal mice following HI insult. HI brain injury was induced in postnatal day 7 (P7) neonatal mice. The pups were administered L-Cysteine (5 mg/kg) at 24, 48, and 72 h post-HI. By conducting TMT-based proteomics analysis, we confirmed that osteopontin (OPN) was the most upregulated protein in ipsilateral cortex 72 h following HI insult. Moreover, OPN was expressed in CD11b&lt;sup>+&lt;/sup>/CD45&lt;sup>low&lt;/sup> cells and infiltrating CD11b&lt;sup>+&lt;/sup>/CD</pubmed_abstract><journal>Acta pharmacologica Sinica</journal><pagination>1658-1669</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9253102</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>L-Cysteine attenuates osteopontin-mediated neuroinflammation following hypoxia-ischemia insult in neonatal mice by inducing S-sulfhydration of Stat3.</pubmed_title><pmcid>PMC9253102</pmcid><pubmed_authors>Liu DX</pubmed_authors><pubmed_authors>Xin DQ</pubmed_authors><pubmed_authors>Yue SW</pubmed_authors><pubmed_authors>Chu XL</pubmed_authors><pubmed_authors>Zhao YJ</pubmed_authors><pubmed_authors>Ke HF</pubmed_authors><pubmed_authors>Li TT</pubmed_authors><pubmed_authors>Wang Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>L-Cysteine attenuates osteopontin-mediated neuroinflammation following hypoxia-ischemia insult in neonatal mice by inducing S-sulfhydration of Stat3.</name><description>We previously show that L-Cysteine administration significantly suppresses hypoxia-ischemia (HI)-induced neuroinflammation in neonatal mice through releasing H&lt;sub>2&lt;/sub>S. In this study we conducted proteomics analysis to explore the potential biomarkers or molecular therapeutic targets associated with anti-inflammatory effect of L-Cysteine in neonatal mice following HI insult. HI brain injury was induced in postnatal day 7 (P7) neonatal mice. The pups were administered L-Cysteine (5 mg/kg) at 24, 48, and 72 h post-HI. By conducting TMT-based proteomics analysis, we confirmed that osteopontin (OPN) was the most upregulated protein in ipsilateral cortex 72 h following HI insult. Moreover, OPN was expressed in CD11b&lt;sup>+&lt;/sup>/CD45&lt;sup>low&lt;/sup> cells and infiltrating CD11b&lt;sup>+&lt;/sup>/CD</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jul</publication><modification>2025-04-26T07:41:08.747Z</modification><creation>2025-04-06T12:22:35.628Z</creation></dates><accession>S-EPMC9253102</accession><cross_references><pubmed>34737419</pubmed><doi>10.1038/s41401-021-00794-2</doi></cross_references></HashMap>