ArticleMolecular medicine reports2018
Dexamethasone inhibits NF‑кBp65 and HMGB1 expression in the pancreas of rats with severe acute pancreatitis.
Article in Molecular medicine reports, 2018. 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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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- Review
- Mitochondria as Inducers of Neutrophil Extracellular Traps.Inflammation · 2026Review
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- HMGB1: key mediator in digestive system diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- The causality between use of glucocorticoids and risk of pancreatitis: a Mendelian randomization study.Frontiers in immunology · 2024Article
- Symmetrical peripheral gangrene: potential mechanisms and therapeutic approaches in severe COVID-19.Frontiers in cardiovascular medicine · 2023Review
- As a Modulator, Multitasking Roles of SIRT1 in Respiratory Diseases.Immune network · 2022Review
- miR-340-5p inhibits pancreatic acinar cell inflammation and apoptosis via targeted inhibition of HMGB1.Experimental and therapeutic medicine · 2022Article
- Intracellular translocation of HMGB1 is important for Zika virus replication in Huh7 cells.Scientific reports · 2022Article
- Mesenteric Lymph Duct Ligation Alleviates Acute Lung Injury Caused by Severe Acute Pancreatitis Through Inhibition of High Mobility Group Box 1-Induced Inflammation in Rats.Digestive diseases and sciences · 2021Article
- Calycosin attenuates severe acute pancreatitis-associated acute lung injury by curtailing high mobility group box 1 - induced inflammation.World journal of gastroenterology · 2021Article
- Glucocorticoids in acute pancreatitis: a propensity score matching analysis.BMC gastroenterology · 2021Article
- miR-9 alleviated the inflammatory response and apoptosis in caerulein-induced acute pancreatitis by regulating FGF10 and the NF-κB signaling pathway.Experimental and therapeutic medicine · 2021Article
- Corticosteroid treatment for acute/acute-on-chronic experimental and naturally occurring pancreatitis in several species: a scoping review to inform possible use in dogs.Acta veterinaria Scandinavica · 2021Article
- Drug discovery and formulation development for acute pancreatitis.Drug delivery · 2020Review
- Neutrophil Extracellular Traps (NETs) and Damage-Associated Molecular Patterns (DAMPs): Two Potential Targets for COVID-19 Treatment.Mediators of inflammation · 2020Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute pancreatitis (SAP) starts as a local inflammation of pancreatic tissue that induces the development of multiple extra‑pancreatic organ dysfunction; however, the underlying mechanisms remain unclear. The present study was designed to evaluate the effect of dexamethasone (DXM) on pancreatic damage and to investigate the role of high‑mobility group box‑1 (HMGB1) and nuclear factor‑κB (NF‑κBp65) in the development of SAP in animal and cell models. For the in vivo experiment, 35 Sprague‑Dawley rats were randomly assigned to three groups: The sham‑operation control group, the SAP group and the DXM treatment group. Histological analysis revealed that, when DXM was infused into SAP rats, edema formation and structural alterations with necrosis were reduced, and the number of apoptotic cells was markedly reduced. In addition, compared with the SAP group, the expression level of HMGB1 was significantly decreased in the nucleus and the expression level of NF‑κBp65 was significantly decreased in the cytoplasm from rats treated with DXM. In vitro, DXM was able to suppress the apoptosis and cell death induced by caerulein (CAE), and DXM could suppress the expression of NF‑κBp65 and HMGB1 induced by CAE, as demonstrated by western blotting and immunofluorescence analysis. Therefore, these results provide an experimental basis for investigating the underlying therapeutic mechanisms of DXM treatment for SAP.
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