ArticleDigestive diseases and sciences2010
Antioxidant inhibits HMGB1 expression and reduces pancreas injury in rats with severe acute pancreatitis.
Article in Digestive diseases and sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Correlation between serum levels of high mobility group box-1 protein and pancreatitis: a meta-analysis.BioMed research international · 2015Pooled it
- A Role for High Mobility Group Box 1 (HMGB1) Release in the Pathogenesis of Gastroesophageal Reflux Disease.Neurogastroenterology and motility · 2025Article
- Anti-DAMP therapies for acute inflammation.Frontiers in immunology · 2025Review
- Oxidative stress and acute pancreatitis (Review).Biomedical reports · 2024Review
- Eugenol Reduced ΜPO, CD45 and HMGB1 Expression and Attenuated the Expression of Leukocyte Infiltration Markers in the Intestinal Tissue in Biliopancreatic Duct Ligation-Induced Pancreatitis in Rats.Medicina (Kaunas, Lithuania) · 2023Article
- The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022Review
- miR-340-5p inhibits pancreatic acinar cell inflammation and apoptosis via targeted inhibition of HMGB1.Experimental and therapeutic medicine · 2022Article
- Damage associated molecular patterns and neutrophil extracellular traps in acute pancreatitis.Frontiers in cellular and infection microbiology · 2022Review
- The role of IL-6 in coronavirus, especially in COVID-19.Frontiers in pharmacology · 2022Review
- NLRP3 Inflammasome-Mediated Inflammation in Acute Pancreatitis.International journal of molecular sciences · 2020Review
- The Dual Role of HMGB1 in Pancreatic Cancer.Journal of pancreatology · 2018Article
- Dexamethasone inhibits NF‑кBp65 and HMGB1 expression in the pancreas of rats with severe acute pancreatitis.Molecular medicine reports · 2018Article
- Augmenter of liver regeneration (ALR) regulates acute pancreatitis via inhibiting HMGB1/TLR4/NF-κB signaling pathway.American journal of translational research · 2018Article
- Emodin alleviates severe acute pancreatitis-associated acute lung injury by decreasing pre-B-cell colony-enhancing factor expression and promoting polymorphonuclear neutrophil apoptosis.Molecular medicine reports · 2017Article
- Expression pattern of HMGB1 and its association with autophagy in acute necrotizing pancreatitis.Molecular medicine reports · 2016Article
- TLR4-mediated NF-κB signaling pathway mediates HMGB1-induced pancreatic injury in mice with severe acute pancreatitis.International journal of molecular medicine · 2016Article
- Sodium Butyrate Reduces Organ Injuries in Mice with Severe Acute Pancreatitis Through Inhibiting HMGB1 Expression.Digestive diseases and sciences · 2015Article
- High-mobility group box 1 protein and its role in severe acute pancreatitis.World journal of gastroenterology · 2015Review
- Spatial and temporal differences of HMGB1 expression in the pancreas of rats with acute pancreatitis.International journal of clinical and experimental pathology · 2015Article
- HMGB1 in health and disease.Molecular aspects of medicine · 2014Review
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
backgroundPathogenesis of severe acute pancreatitis is still unclear, which leads to a lack of proper treatment in severe acute pancreatitis therapeutic strategy.
objectiveTo investigate the effect of treatment with antioxidant pyrrolidine dithiocarbamate on pancreas injury in rats with severe acute pancreatitis and its possible mechanism.
methodsA total of 144 male Sprague-Dawley rats were randomly allocated into a sham operation group (n=48), a severe acute pancreatitis group (n=48), and a pyrrolidine dithiocarbamate-treated group (n=48). All the rats were killed at 1, 3, 6, 12, 24, and 48 h after operation. The pancreas histopathologies were observed and serum amylase levels were tested. Meanwhile, the nuclear factor-kappaB activation, tumor necrosis factor-alpha levels and high-mobility group box protein-1 expression levels in pancreatic tissue were studied.
resultsAnimals receiving pyrrolidine dithiocarbamate had significantly improved pancreas histopathology and lower serum amylase levels (p<0.05). In the severe acute pancreatitis group, pancreas tumor necrosis factor-alpha levels reached a peak at 6 h after operation and afterwards rapidly declined to normal levels. However, high-mobility group box protein-1 levels in pancreatic tissue increased remarkably at the 12th hour, reached a peak at 24 h, and maintained up to 48 h post-severe acute pancreatitis. Compared to the severe acute pancreatitis group, the pancreas nuclear factor-kappaB activity, tumor necrosis factor-alpha, high-mobility group box protein-1 levels in the pyrrolidine dithiocarbamate-treated group all remarkably decreased (p<0.05).
conclusionsHigh-mobility group box protein-1 seems to act as a late cytokine mediator in the pathogenesis of severe acute pancreatitis. Pyrrolidine dithiocarbamate might inhibit the activation of nuclear factor-kappaB to blockade tumor necrosis factor-alpha, thereby indirectly suppressing the high-mobility group box protein-1 and reducing pancreatic tissue damage in rats with severe acute pancreatitis.
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