Our research aimed to investigate whether soluble thrombomodulin (sTM) relieved Diquat (DQ)-induced acute kidney injury (AKI) via HMGB1/IκBα/NF-κB signaling pathways. An AKI rat model was constructed using DQ. Pathological changes in renal tissue were detected by HE and Masson staining. Gene expression was determined using qRT-PCR, IHC, and western blotting. Cell activity and apoptosis were analysed using CCK-8 and Flow cytometry, respectively. An abnormal kidney structure was observed in DQ rats. The levels of blood urea nitrogen (BUN), creatinine (CRE), uric acid (UA), oxidative stress, and inflammatory responses in the DQ group increased on the 7th day but decreased on the 14th day, compared with the control group. Additionally, HMGB1, sTM, and NF-kappaB (NF-κB) expression had increased in the DQ group compared with the control group, while the IκKα and IκB-α levels had decreased. In addition, sTM relieved the damaging effects of diquat on renal tubular epithelial cell viability, apoptosis, and the inflammatory response. The levels of HMGB1, TM, and NF-κB mRNA and protein were significantly decreased in the DQ + sTM group compared with the DQ group. These findings indicated that sTM could relieve Diquat-induced AKI through HMGB1/IκBα/NF-κB signaling pathways, which provides a treatment strategy for Diquat-induced AKI.
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http://dx.doi.org/10.1016/j.fct.2023.113871 | DOI Listing |
Acta Anaesthesiol Scand
January 2025
CAG Center for Endotheliomics, Department of Clinical Immunology, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark.
Background: Acute respiratory failure (ARF) is common in critically ill patients, and 50% of patients in intensive care units require mechanical ventilation [3, 4]. The COVID-19 pandemic revealed that COVID-19 infection induced ARF caused by damage to the microvascular pulmonary endothelium. In a randomized clinical trial, mechanically ventilated COVID-19 patients with severe endotheliopathy, as defined by soluble thrombomodulin (sTM) ≥ 4 ng/mL, were randomized to evaluate the effect of a 72-h infusion of low-dose prostacyclin 1 ng/kg/min or placebo.
View Article and Find Full Text PDFProc Jpn Acad Ser B Phys Biol Sci
December 2024
Professor, Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, Suzuka, Mie, Japan.
Thrombomodulin (TM) is an important regulator of intravascular blood coagulation and inflammation. TM inhibits the procoagulant and proinflammatory activities of thrombin and promotes the thrombin-induced activation of protein C (PC) bound to the endothelial PC receptor (EPCR). Activated PC (APC) inactivates coagulation factors Va and VIIIa, thereby inhibiting blood clotting.
View Article and Find Full Text PDFJ Surg Res
December 2024
Firefighters' Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, District of Columbia; Department of Biochemistry and Molecular & Cellular Biology, Georgetown University School of Medicine, Washington, District of Columbia; Department of Surgery, Georgetown University School of Medicine, Washington, District of Columbia; The Burn Center, Department of Surgery, MedStar Washington Hospital Center, Washington, District of Columbia; Department of Plastic and Reconstructive Surgery, Georgetown University School of Medicine, Washington, District of Columbia. Electronic address:
J Diabetes Complications
November 2024
Steno Diabetes Center Copenhagen, Herlev, Denmark; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark.
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