ArticleInflammation2022
Ulinastatin Alleviates Rhabdomyolysis-Induced Acute Kidney Injury by Suppressing Inflammation and Apoptosis via Inhibiting TLR4/NF-κB Signaling Pathway.
Article in Inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 17 citations in OpenAlex.
- Protective effect of ulinastatin against negative inflammatory response and organ dysfunction in acute aortic dissection surgery: The PANDA trial.Cell reports. Medicine · 2025Trial
- The impact of ulinastatin on lymphocyte apoptosis and autophagy in sepsis patients.Scientific reports · 2024Trial
- Stress-Dependent NF-κB Signaling in Acute Kidney Injury: Linking Inflammation, Autophagy, and Apoptosis.International journal of molecular sciences · 2026Review
- The impact of ulinastatin on postoperative clinical outcomes in patients with gastric cancer: a retrospective cohort analysis.Journal of gastrointestinal oncology · 2026Article
- Treatment protocol for pneumonia with acute kidney injury: effects of ulinastatin combined with CRRT on inflammatory factors and renal function in patients.Frontiers in medicine · 2026Article
- Protective effect of Panax ginseng extract on cisplatin-induced AKI via downregulating cell death associated genes.Scientific reports · 2025Article
- Article
- Effect of octreotide combined with ulinastatin on the creatinine-to-albumin ratio and systemic immune-inflammation index in patients with severe acute pancreatitis.American journal of translational research · 2025Article
- Nephroprotective effects of substances of medicine food homology and traditional Chinese medicine phytochemicals against acute kidney injury.Frontiers in pharmacology · 2025Review
- Article
- Ulinastatin attenuates renal fibrosis by regulating AMPK/HIF-1α signaling pathway-mediated glycolysis.Scientific reports · 2024Article
- New Therapeutic Method for Alleviating Damage of Acute Kidney Injury ThroughInternational journal of molecular sciences · 2024Article
- Engineered urolithin A-laden functional polymer-lipid hybrid nanoparticles prevent cisplatin-induced proximal tubular injury in vitro.European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V · 2024Article
- Telbivudine-induced rhabdomyolysis in a patient undergoing haemodialysis: A case report and review of literature.The Journal of international medical research · 2023Review
- Continuous Monochromatic Blue Light Exacerbates High-Fat Diet-Induced Kidney Injury via Corticosterone-Mediated Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Article
- Ulinastatin combined with somatostatin enhances disease control and modulates serum inflammatory factors in patients with severe pancreatitis.American journal of translational research · 2023Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Acute kidney injury (AKI) is an important complication of rhabdomyolysis (RM), but there is lack of effective treatments. Ulinastatin (UTI) is a broad-spectrum serine protease inhibitor isolated and purified from human urine with strong anti-inflammatory and cytoprotective actions. The aim of this research was to investigate the effect and potential mechanism of UTI on RM-induced AKI (RM-AKI). We established RM-induced AKI model and myoglobin (Mb)-stimulated NRK-52E cell model. In vivo, twenty-four rats were randomly divided into three groups (n = 8): control, RM-AKI, and RM-AKI + UTI. In vitro, the NRK-52E cells were divided into six groups according to the different treatment method. Mb-stimulated NRK-52E cells were treated with UTI or si-TLR4 transfection to characterize the mechanisms of UTI in RM-AKI. Indicators of the kidney injury, cell viability, cell cycle, oxidative stress, inflammation, apoptosis, and TLR4/NF-κB signaling pathway were assessed. In vivo and in vitro, UTI significantly decreased the expression of TLR4 and p65. In vivo, UTI significantly improved renal function and reduced inflammatory reaction and kidney injury. In vitro, UTI protected NRK-52E cells from Mb stimulation by suppressing cell cytotoxicity, cell cycle inhibition, overproduction of ROS, inflammation, and apoptosis. Additionally, UTI played a protective role by downregulating the TLR4 expression. The results indicate that UTI alleviates RM-AKI by suppressing the inflammatory response and apoptosis via inhibiting TLR4/NF-κB signaling pathway. Our study provides a new mechanism for the protective effect of UTI on RM-AKI.
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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.