ArticleInternational journal of molecular sciences2015
Exogenous Carbon Monoxide Decreases Sepsis-Induced Acute Kidney Injury and Inhibits NLRP3 Inflammasome Activation in Rats.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 78 citations in OpenAlex.
- Role of oxidative stress in sepsis: Mechanisms, pathways, and therapeutic strategies.Journal of pharmaceutical analysis · 2026Review
- Luteoloside ameliorates sepsis-induced acute lung injury via AMPK-ULK1 pathway-mediated autophagy.Histology and histopathology · 2025Article
- Trans-Coumaryl acetate mediates GRK5/NF-κB/Nrf2 signaling axis to ameliorate septic acute kidney injury.Journal of cell communication and signaling · 2025Article
- CORM-A1 Alleviates Pro-Atherogenic Manifestations via miR-34a-5p Downregulation and an Improved Mitochondrial Function.Antioxidants (Basel, Switzerland) · 2023Article
- Protective Effect of Silymarin on Liver in Experimental in the Sepsis Model of Rats.Acta histochemica et cytochemica · 2023Article
- Mitochondrial protective effects caused by the administration of mefenamic acid in sepsis.Journal of neuroinflammation · 2022Article
- Novel insights into NOD-like receptors in renal diseases.Acta pharmacologica Sinica · 2022Review
- Ambient carbon monoxide correlates with mortality risk of hemodialysis patients: comparing results of control selection in the case-crossover designs.Kidney research and clinical practice · 2022Article
- Gases in Sepsis: Novel Mediators and Therapeutic Targets.International journal of molecular sciences · 2022Review
- Article
- Liposomal Artificial Red Blood Cell-Based Carbon Monoxide Donor Is a Potent Renoprotectant against Cisplatin-Induced Acute Kidney Injury.Pharmaceutics · 2021Article
- Platelet Inhibition Prevents NLRP3 Inflammasome Activation and Sepsis-Induced Kidney Injury.International journal of molecular sciences · 2021Article
- Nature's marvels endowed in gaseous molecules I: Carbon monoxide and its physiological and therapeutic roles.Acta pharmaceutica Sinica. B · 2021Review
- Emerging mechanisms of immunocoagulation in sepsis and septic shock.Trends in immunology · 2021Review
- Significance of Heme and Heme Degradation in the Pathogenesis of Acute Lung and Inflammatory Disorders.International journal of molecular sciences · 2021Review
- MIR210HG Aggravates Sepsis-Induced Inflammatory Response of Proximal Tubular Epithelial Cell via the NF-κB Signaling Pathway.Yonsei medical journal · 2021Article
- Carbon monoxide-triggered health effects: the important role of the inflammasome and its possible crosstalk with autophagy and exosomes.Archives of toxicology · 2021Review
- Endothelial progenitor cells-derived exosomal microRNA-21-5p alleviates sepsis-induced acute kidney injury by inhibiting RUNX1 expression.Cell death & disease · 2021Article
- Long Non-Coding RNA RMRP Contributes to Sepsis-Induced Acute Kidney Injury.Yonsei medical journal · 2021Article
- Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carbon monoxide (CO) has shown various physiological effects including anti-inflammatory activity in several diseases, whereas the therapeutic efficacy of CO on sepsis-induced acute kidney injury (AKI) has not been reported as of yet. The purpose of the present study was to explore the effects of exogenous CO on sepsis-induced AKI and nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome activation in rats. Male rats were subjected to cecal ligation and puncture (CLP) to induce sepsis and AKI. Exogenous CO delivered from CO-releasing molecule 2 (CORM-2) was used intraperitoneally as intervention after CLP surgery. Therapeutic effects of CORM-2 on sepsis-induced AKI were assessed by measuring serum creatinine (Scr) and blood urea nitrogen (BUN), kidney histology scores, apoptotic cell scores, oxidative stress, levels of cytokines TNF-α and IL-1β, and NLRP3 inflammasome expression. CORM-2 treatment protected against the sepsis-induced AKI as evidenced by reducing serum Scr/BUN levels, apoptotic cells scores, increasing survival rates, and decreasing renal histology scores. Furthermore, treatment with CORM-2 significantly reduced TNF-α and IL-1β levels and oxidative stress. Moreover, CORM-2 treatment significantly decreased NLRP3 inflammasome protein expressions. Our study provided evidence that CORM-2 treatment protected against sepsis-induced AKI and inhibited NLRP3 inflammasome activation, and suggested that CORM-2 could be a potential therapeutic candidate for treating sepsis-induced AKI.
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