ArticleBMC nephrology2025
Ursodeoxycholic acid protects against sepsis-induced acute kidney injury by activating Nrf2/HO-1 and inhibiting NF-κB pathway.
Article in BMC nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Folate-Targeted Co-Delivery of Curcumin and siRela Nanoparticles Synergistically Treat Sepsis-Associated Acute Kidney Injury.ACS omega · 2026Article
- Azilsartan as a novel anti-ferriptotic agent via the upregulation of the Nrf2/HO-1/SLC7A11/GPX4 axis and downregulation of inflammatory pathways in folic acid-induced acute kidney injury in male mice.Toxicology reports · 2026Article
- Ureic clearance granule ameliorates chronic kidney disease by reshaping microbial dysbiosis via modulating bile acid metabolism.Chinese medicine · 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
- Exercise stress and tissue remodeling: advances in exosome-mediated RNA-RBP networks in musculoskeletal injury repair and functional recovery.Frontiers in genetics · 2026Review
- Bile acid dysregulation in sepsis: mechanisms, clinical implications, and future perspectives.Frontiers in cellular and infection microbiology · 2026Review
- Oxidative stress and endoplasmic reticulum stress in acute kidney injury: mechanistic crosstalk and therapeutic modulation.Frontiers in medicine · 2026Review
- Protective Effect of Hepcidin on Sepsis-Associated Acute Kidney Injury via Activating the Nrf2/GPX4 Signaling Pathway.Current issues in molecular biology · 2025Article
- miR-769-5p has diagnostic value in acute kidney injury in intensive care unit patients and mediates disease development by targeting SIRT6.BMC nephrology · 2025Article
- Plasma Bile Acid Profiling Reveals Novel Early Diagnostic Biomarkers for Pediatric Sepsis.Journal of inflammation research · 2025Article
- Post-translational modifications in sepsis-induced acute kidney injury: mechanisms and perspectives.Frontiers in pharmacology · 2025Review
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6 authors.
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Abstract
backgroundUrsodeoxycholic acid (UDCA), traditionally recognized for its hepatoprotective effects, has also shown potential in protecting kidney injury. This study aimed to evaluate the protective effects of UDCA against sepsis-induced acute kidney injury (AKI) and to elucidate the underlying mechanisms.
methodsSixty male C57BL/6 N mice were utilized to establish a sepsis-induced AKI model through intravenous injection of lipopolysaccharides (LPS, 10 mg/kg). UDCA (15, 30, and 60 mg/kg) was administered intraperitoneally once daily for 7 days before LPS injection. Kidney injury was evaluated by HE staining and biochemical markers, including serum creatinine (Cr), blood urea nitrogen (BUN), urinary protein, neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), N-acetyl-β-D-glucosaminidase (NAG), and retinol binding protein (RBP). Oxidative stress parameters and nuclear factor erythroid 2-related factor 2 (Nrf2)/ heme oxygenase-1 (HO-1) pathway, pro-inflammatory cytokines and nuclear factor-kappa B (NF-κB) pathway were also evaluated. Additionally, HK-2 cells were treated with LPS in vitro, and cell viability and apoptosis were detected using CCK-8 kit and flow cytometer, respectively.
resultsUDCA significantly attenuated LPS-induced renal histopathological damage and improved renal function, as evidenced by reduction in serum Cr, BUN, and urinary protein levels. UDCA also up-regulated the protein expression of zonula occludens-1 (ZO-1) and Ezrin in the kidney, and reduced the urinary levels of NGAL, KIM-1, NAG, and RBP. Moreover, UDCA inhibited NF-κB p65 phosphorylation and reduced pro-inflammatory cytokines levels (TNF-α, IL-1β, and IL-6) in both serum and kidney. UDCA alleviated oxidative stress by activating the Nrf2/HO-1 pathway in the kidney. In vitro, UDCA reduced LPS-induced cell injury and apoptosis in HK-2 cells, with these protective effects being blocked by the Nrf2 inhibitor ML385.
conclusionsOur present study demonstrated that UDCA exerts protective effects against sepsis-induced AKI by attenuating oxidative stress and inflammation, primarily through the activation of the Nrf2/HO-1 pathway and inhibition of the NF-κB pathway. These findings highlight the therapeutic potential of UDCA in preventing sepsis-induced AKI.
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