ArticleMolecular and cellular biochemistry2025
Ursodeoxycholic and chenodeoxycholic bile acids attenuate systemic and liver inflammation induced by lipopolysaccharide in rats.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 11 citations in OpenAlex.
- Obeticholic acid attenuates complete freund's adjuvant-induced arthritis in rats through FXR-mediated modulation of TGF-β/TAK1/MKK3/p38 MAPK signaling, inflammation, and oxidative stress.Inflammopharmacology · 2026Article
- Ursodeoxycholic Acid Attenuates Lipopolysaccharide-Induced Myocardial Injury by Inhibiting Oxidative Stress, Inflammation, and Apoptosis: The Interplay of Sirt1/Nrf2 and Akt/NF-κB Signaling Pathways.International journal of molecular sciences · 2026Article
- The Endogenous Metabolite TDCA Ameliorates LPS-Driven Liver Injury via Modulation of Caspase-11/GSDMD-Mediated Pyroptosis.International journal of molecular sciences · 2026Article
- Chenodeoxycholic acid suppresses colorectal cancer by activating Farnesoid X receptor.American journal of cancer research · 2026Article
- Bile acid dysregulation in sepsis: mechanisms, clinical implications, and future perspectives.Frontiers in cellular and infection microbiology · 2026Review
- Therapeutical progress in sepsis-induced cardiomyopathy.Frontiers in cardiovascular medicine · 2026Review
- Ursodeoxycholic acid as a potential cardioprotective agent: molecular mechanisms, experimental evidence, and clinical perspectives.Frontiers in pharmacology · 2026Review
- Protective Effect of Obeticholic Acid on Sepsis-Induced Liver Dysfunction via Regulating Bile Acid Homeostasis.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Goose Deoxycholic Acid Ameliorates Liver Injury in Laying Hens with Fatty Liver Hemorrhage Syndrome by Inhibiting the Inflammatory Response.International journal of molecular sciences · 2025Article
- Ursodeoxycholic and chenodeoxycholic bile acids alleviate endotoxininduced acute lung injury in rats by modulating aquaporin expression and pathways associated with apoptosis and inflammation.Frontiers in pharmacology · 2025Article
- Cardioprotective Effects of Ursodeoxycholic Acid in Isoprenaline-Induced Myocardial Injury in Rats.Biomolecules · 2024Article
- Polyphenol-RichFoods (Basel, Switzerland) · 2024Article
- NLRP3 Inflammasome and Gut Dysbiosis Linking Diabetes Mellitus and Inflammatory Bowel Disease.Archives of internal medicine research · 2024Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacterial lipopolysaccharide (LPS) induces general inflammation, by activating pathways involving cytokine production, blood coagulation, complement system activation, and acute phase protein release. The key cellular players are leukocytes and endothelial cells, that lead to tissue injury and organ failure. The aim of this study was to explore the anti-inflammatory, antioxidant, and cytoprotective properties of two bile acids, ursodeoxycholic acid (UDCA) and chenodeoxycholic acid (CDCA) in LPS-induced endotoxemia in rats. The experiment involved six distinct groups of Wistar rats, each subjected to different pretreatment conditions: control and LPS groups were pretreated with propylene glycol, as a bile acid solvent, while the other groups were pretreated with UDCA or CDCA for 10 days followed by an LPS injection on day 10. The results showed that both UDCA and CDCA reduced the production of pro-inflammatory cytokines: TNF-α, GM-CSF, IL-2, IFNγ, IL-6, and IL-1β and expression of nuclear factor-κB (NF-κB) induced by LPS. In addition, pretreatment with these bile acids showed a positive impact on lipid profiles, a decrease in ICAM levels, an increase in antioxidant activity (SOD, |CAT, GSH), and a decrease in prooxidant markers (H
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.