ArticleBioengineered2022
Combination therapy of Ulinastatin with Thrombomodulin alleviates endotoxin (LPS) - induced liver and kidney injury via inhibiting apoptosis, oxidative stress and HMGB1/TLR4/NF-κB pathway.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- [Protective effect of ulinastatin combined with dexmedetomidine against hepatic ischemia-reperfusion injury in laparoscopic hepatectomy for liver cancer and cirrhosis: a randomized controlled trial].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Trial
- The impact of ulinastatin on postoperative clinical outcomes in patients with gastric cancer: a retrospective cohort analysis.Journal of gastrointestinal oncology · 2026Article
- Role of oxidative stress in sepsis: Mechanisms, pathways, and therapeutic strategies.Journal of pharmaceutical analysis · 2026Review
- α-AMA induced liver failure is associated with elevation of HMGB1 lactylation modification in mice.BMC gastroenterology · 2026Article
- Comparative renoprotective effects of phoenixin-14, a novel peptide, and dexamethasone in LPS-induced sepsis: targeting inflammation, oxidative stress, and apoptosis.Apoptosis : an international journal on programmed cell death · 2026Article
- Mitigation of sepsis-associated acute kidney injury by thymoquinone via targeting pyroptosis and attenuation of inflammation in C57BL/6 mice.Iranian journal of basic medical sciences · 2026Article
- The Multifaceted Roles of Thrombomodulin: Anti-coagulation, Anti-inflammation, and Anti-tumor Potential.Current pharmaceutical design · 2025Review
- Targeting PANoptosis in Bacterial-Induced Inflammatory Diseases: Mechanisms and Therapeutic Interventions.Journal of inflammation research · 2025Review
- Neoastilbin ameliorates sepsis-induced liver and kidney injury by blocking the TLR4/NF-κB pathway.Histology and histopathology · 2024Article
- Neuroprotective effects of ulinastatin on Escherichia coli meningitis rats through inhibiting PKCα phosphorylation and reducing zonula occludens-1 degradation.Scientific reports · 2024Article
- Dihydromyricetin Nanoparticles Alleviate Lipopolysaccharide-Induced Acute Kidney Injury by Decreasing Inflammation and Cell Apoptosis via the TLR4/NF-κB Pathway.Journal of functional biomaterials · 2024Article
- Diterpenoid Tanshinones Can Inhibit Lung Cancer Progression by Improving the Tumor Microenvironment and Downregulation of NF-κB Expression.ACS omega · 2024Article
- Revealing the role of Peg13: A promising therapeutic target for mitigating inflammation in sepsis.Genetics and molecular biology · 2024Article
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- Exploring and Validating the Mechanism of Ulinastatin in the Treatment of Sepsis-Associated Encephalopathy Based on Transcriptome Sequencing.Journal of inflammation research · 2024Article
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- Article
- Activation of Kupffer cells in NAFLD and NASH: mechanisms and therapeutic interventions.Frontiers in cell and developmental biology · 2023Review
- Hepatoprotective Effect of Silver Nanoparticles at Two Different Particle Sizes: Comparative Study with and without Silymarin.Current issues in molecular biology · 2022Article
- Determination of HMGB1 in hepatitis B virus-related acute-on-chronic liver failure patients with acute kidney injury: Early prediction and prognostic implications.Frontiers in pharmacology · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a type of systemic inflammation response syndrome that leads to organ function disorders. Currently, there is no specific medicine for sepsis in clinical practice. Lipopolysaccharide (LPS) is an important endotoxin that causes sepsis. Here, we report an effective two-drug combination therapy to treat LPS-induced liver and kidney injury in endotoxic rats. Ulinastatin (UTI) and Thrombomodulin (TM) are biological macromolecules extracted from urine. In our study, combination therapy significantly improved LPS-induced liver and kidney pathological structure and functional injury, and significantly improved the survival rate of endotoxic rats. Results of TUNEL staining and Western blot showed that UTI combined with TM inhibited the excessive apoptosis of liver and kidney cells caused by LPS. The drug combination also promoted the proliferation of liver and kidney cells, reduced the levels of pro-inflammatory factors interleukin (IL)-6, IL-1β, tumor or necrosis factor (TNF)-α and nitric oxide, and down-regulated the expression of High Mobility Group Box 1 (HMGB1), Toll-like receptor (TLR) 4 and Nuclear Factor (NF)-κB phosphorylation to inhibit inflammation. In addition, the combination of UTI and TM also promoted the production of a variety of antioxidant enzymes in the tissues and inhibited the production of lipid peroxidation malondialdehyde (MDA) to enhance antioxidant defenses. Our experiments also proved that UTI combined with TM did not reduce the anticoagulant effect of TM. These results suggested that UTI combined with TM can improve endotoxin-induced liver and kidney damage and mortality by inhibiting liver and kidney cell apoptosis, promoting proliferation, and inhibiting inflammation and oxidative injury.
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