<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lim JS</submitter><funding>Ministry of Education</funding><funding>Korea Food Research Institute (KFRI) funded by the Ministry of Science</funding><funding>National Research Foundation of Korea (NRF)</funding><funding>Ministry of Science</funding><funding>Korea Research Institute of Bioscience and Biotechnology (KRIBB) Research Initiative Program</funding><funding>National Research Foundation of Korea</funding><pagination>1792</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10604099</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(10)</volume><pubmed_abstract>&lt;i>Ehretia tinifolia&lt;/i> (&lt;i>E. tinifolia&lt;/i>) L., an evergreen tree with substantial biological activity, including antioxidant and anti-inflammatory effects, has been used in many herbal and traditional medicines. To elucidate its antioxidant and anti-inflammatory activity and the underlying mechanisms, we applied a methanol extract of &lt;i>E. tinifolia&lt;/i> (ETME) to lipopolysaccharide (LPS)-stimulated mouse immortalized Kupffer cells. ETME suppressed the LPS-induced increase in nitric oxide, a mediator for oxidative stress and inflammation, and restored LPS-mediated depletion of total glutathione level by stabilizing antioxidative nuclear factor erythroid 2-related factor 2 (Nrf2) and the subsequent increase in heme oxygenase-1 levels. Furthermore, ETME inhibited the LPS-induced productio</pubmed_abstract><journal>Antioxidants (Basel, Switzerland)</journal><pubmed_title>Inhibitory Effects of &lt;i>Ehretia tinifolia&lt;/i> Extract on the Excessive Oxidative and Inflammatory Responses in Lipopolysaccharide-Stimulated Mouse Kupffer Cells.</pubmed_title><pmcid>PMC10604099</pmcid><funding_grant_id>Main Research Program E0210300</funding_grant_id><funding_grant_id>NRF-2020R1C1C1007261</funding_grant_id><funding_grant_id>E0210300</funding_grant_id><funding_grant_id>NRF-2022R1I1A1A01056975</funding_grant_id><funding_grant_id>KGM5242322</funding_grant_id><pubmed_authors>Cho YC</pubmed_authors><pubmed_authors>Lim JS</pubmed_authors><pubmed_authors>Lee DY</pubmed_authors><pubmed_authors>Yun H</pubmed_authors><pubmed_authors>Lee SH</pubmed_authors><pubmed_authors>Bach TT</pubmed_authors><pubmed_authors>Cho N</pubmed_authors><pubmed_authors>Choi JU</pubmed_authors><pubmed_authors>Yoo G</pubmed_authors><pubmed_authors>Lee KY</pubmed_authors><pubmed_authors>Park SJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Inhibitory Effects of &lt;i>Ehretia tinifolia&lt;/i> Extract on the Excessive Oxidative and Inflammatory Responses in Lipopolysaccharide-Stimulated Mouse Kupffer Cells.</name><description>&lt;i>Ehretia tinifolia&lt;/i> (&lt;i>E. tinifolia&lt;/i>) L., an evergreen tree with substantial biological activity, including antioxidant and anti-inflammatory effects, has been used in many herbal and traditional medicines. To elucidate its antioxidant and anti-inflammatory activity and the underlying mechanisms, we applied a methanol extract of &lt;i>E. tinifolia&lt;/i> (ETME) to lipopolysaccharide (LPS)-stimulated mouse immortalized Kupffer cells. ETME suppressed the LPS-induced increase in nitric oxide, a mediator for oxidative stress and inflammation, and restored LPS-mediated depletion of total glutathione level by stabilizing antioxidative nuclear factor erythroid 2-related factor 2 (Nrf2) and the subsequent increase in heme oxygenase-1 levels. Furthermore, ETME inhibited the LPS-induced productio</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Sep</publication><modification>2026-06-22T03:21:57.989Z</modification><creation>2025-04-04T10:07:01.89Z</creation></dates><accession>S-EPMC10604099</accession><cross_references><pubmed>37891872</pubmed><doi>10.3390/antiox12101792</doi></cross_references></HashMap>