<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>43(3)</volume><submitter>Yang Z</submitter><pubmed_abstract>&lt;h4>Objective&lt;/h4>To investigate the therapeutic mechanism of diosmetin on 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-induced Crohn's disease (CD)-like colitis in mice.&lt;h4>Methods&lt;/h4>Wild-type C57BL/6 mice were randomized into control group, TNBS-induced CD-like colitis group (TNBS group) and 50 mg·kg&lt;sup>-1&lt;/sup>·d&lt;sup>-1&lt;/sup> diosmetin-treated group (&lt;i>n&lt;/i>=8). Disease activity (DAI) scores, body weight changes, histological scores, colon lengths and colon mucosal levels of TNF-α, IFN-γ, and IL-17A were measured to evaluate the severity of colitis. The changes of T lymphocyte subsets (Th1/Th2 and Th17/Treg) in the mesenteric lymph nodes were analyzed by flow cytometry. Network pharmacology and molecular docking were used to analyze the effect of diosmetin on PI3K/AKT pathway.&lt;h4>Re</pubmed_abstract><journal>Nan fang yi ke da xue xue bao = Journal of Southern Medical University</journal><pagination>474-482</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10122747</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>[Diosmetin regulates intestinal immune balance by inhibiting PI3K/AKT signaling to relieve 2, 4, 6-trinitrobenzene sulfonic acid-induced Crohn's disease-like colitis in mice].</pubmed_title><pmcid>PMC10122747</pmcid><pubmed_authors>Ge S</pubmed_authors><pubmed_authors>Yang Z</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Zhao T</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Zuo L</pubmed_authors><pubmed_authors>Zhou Y</pubmed_authors><pubmed_authors>Cheng Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>[Diosmetin regulates intestinal immune balance by inhibiting PI3K/AKT signaling to relieve 2, 4, 6-trinitrobenzene sulfonic acid-induced Crohn's disease-like colitis in mice].</name><description>&lt;h4>Objective&lt;/h4>To investigate the therapeutic mechanism of diosmetin on 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-induced Crohn's disease (CD)-like colitis in mice.&lt;h4>Methods&lt;/h4>Wild-type C57BL/6 mice were randomized into control group, TNBS-induced CD-like colitis group (TNBS group) and 50 mg·kg&lt;sup>-1&lt;/sup>·d&lt;sup>-1&lt;/sup> diosmetin-treated group (&lt;i>n&lt;/i>=8). Disease activity (DAI) scores, body weight changes, histological scores, colon lengths and colon mucosal levels of TNF-α, IFN-γ, and IL-17A were measured to evaluate the severity of colitis. The changes of T lymphocyte subsets (Th1/Th2 and Th17/Treg) in the mesenteric lymph nodes were analyzed by flow cytometry. Network pharmacology and molecular docking were used to analyze the effect of diosmetin on PI3K/AKT pathway.&lt;h4>Re</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Mar</publication><modification>2025-04-04T10:22:15.394Z</modification><creation>2025-02-19T02:39:05.205Z</creation></dates><accession>S-EPMC10122747</accession><cross_references><pubmed>37087594</pubmed><doi>10.12122/j.issn.1673-4254.2023.03.19</doi></cross_references></HashMap>