<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>46(1)</volume><submitter>Xia YM</submitter><pubmed_abstract>&lt;h4>Objective&lt;/h4>This study was designed to observe the effect of toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) pathway activity on sepsis-associated acute kidney injury (SA-AKI), thereby providing new considerations for the prevention and treatment of SA-AKI.&lt;h4>Methods&lt;/h4>The rats were divided into Sham, cecal ligation and puncture (CLP), CLP + vehicle, and CLP + TAK-242 groups. Except the Sham group, a model of CLP-induced sepsis was established in other groups. After 24 h, the indicators related to kidney injury in blood samples were detected. The pathological changes in the kidneys were observed by hematoxylin-eosin staining, and tubular damage was scored. Oxidative stress-related factors, mitochondrial dysfunction-related indicators in each group were measured; the lev</pubmed_abstract><journal>Renal failure</journal><pagination>2313176</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10877656</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>TAK-242 improves sepsis-associated acute kidney injury in rats by inhibiting the TLR4/NF-κB signaling pathway.</pubmed_title><pmcid>PMC10877656</pmcid><pubmed_authors>Wu WD</pubmed_authors><pubmed_authors>Liang JF</pubmed_authors><pubmed_authors>Guan YQ</pubmed_authors><pubmed_authors>Xia YM</pubmed_authors></additional><is_claimable>false</is_claimable><name>TAK-242 improves sepsis-associated acute kidney injury in rats by inhibiting the TLR4/NF-κB signaling pathway.</name><description>&lt;h4>Objective&lt;/h4>This study was designed to observe the effect of toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) pathway activity on sepsis-associated acute kidney injury (SA-AKI), thereby providing new considerations for the prevention and treatment of SA-AKI.&lt;h4>Methods&lt;/h4>The rats were divided into Sham, cecal ligation and puncture (CLP), CLP + vehicle, and CLP + TAK-242 groups. Except the Sham group, a model of CLP-induced sepsis was established in other groups. After 24 h, the indicators related to kidney injury in blood samples were detected. The pathological changes in the kidneys were observed by hematoxylin-eosin staining, and tubular damage was scored. Oxidative stress-related factors, mitochondrial dysfunction-related indicators in each group were measured; the lev</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2026-07-15T02:44:16.925Z</modification><creation>2026-06-29T03:09:24.441Z</creation></dates><accession>S-EPMC10877656</accession><cross_references><pubmed>38482886</pubmed><doi>10.1080/0886022X.2024.2313176</doi></cross_references></HashMap>