ArticleDigestive diseases and sciences2015
Histone deacetylase regulates trypsin activation, inflammation, and tissue damage in acute pancreatitis in mice.
Article in Digestive diseases and sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 27 citations in OpenAlex.
- Post-translational modification crosstalk in acute pancreatitis: linking acinar stress to innate immune amplification and tissue repair.Frontiers in immunology · 2026Review
- Roles of chemokines in pancreatitis: A review.World journal of gastrointestinal pathophysiology · 2025Review
- Lysine acetylation and its role in the pathophysiology of acute pancreatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Epigenetic small-molecule screen for inhibition and reversal of acinar ductal metaplasia in mouse pancreatic organoids.Frontiers in pharmacology · 2024Article
- Damage associated molecular patterns and neutrophil extracellular traps in acute pancreatitis.Frontiers in cellular and infection microbiology · 2022Review
- Sodium Butyrate Attenuates Taurocholate-Induced Acute Pancreatitis by Maintaining Colonic Barrier and Regulating Gut Microorganisms in Mice.Frontiers in physiology · 2022Article
- Butyrate ameliorates caerulein-induced acute pancreatitis and associated intestinal injury by tissue-specific mechanisms.British journal of pharmacology · 2019Article
- MMP-2 and MMP-9 gene polymorphisms act as biological indicators for ulinastatin efficacy in patients with severe acute pancreatitis.Medicine · 2019Article
- Class I histone deacetylase inhibition improves pancreatitis outcome by limiting leukocyte recruitment and acinar-to-ductal metaplasia.British journal of pharmacology · 2017Article
- Associations ofBioscience reports · 2017Article
- Epigenetic drug discovery: breaking through the immune barrier.Nature reviews. Drug discovery · 2016Review
- Epigenetic Regulation of Interleukin 6 by Histone Acetylation in Macrophages and Its Role in Paraquat-Induced Pulmonary Fibrosis.Frontiers in immunology · 2016Article
- Role of histone deacetylases in pancreas: Implications for pathogenesis and therapy.World journal of gastrointestinal oncology · 2015Review
- Characterization of Mouse Models of Early Pancreatic Lesions Induced by Alcohol and Chronic Pancreatitis.Pancreas · 2015Article
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Authors and funding
4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundThe onset of acute pancreatitis (AP) is characterized by early protease activation followed by inflammation and organ damage, but the mechanisms are poorly understood.
aimsWe hypothesized that histone deacetylase (HDAC) inhibition might exert protective effects on AP and investigated the role of HDAC in trypsin activation, inflammation, and tissue damage in severe AP.
methodsMale C57Bl/6 mice were treated i.p. with the HDAC inhibitor trichostatin A (2 mg/kg) prior to retrograde infusion of taurocholic acid (5 %) into the pancreatic duct. Serum levels of amylase and interleukin (IL)-6, pancreatic levels of macrophage inflammatory protein-2 (MIP-2) as well as tissue morphology and myeloperoxidase activity in the pancreas and lung were determined 24 h after taurocholate challenge. Trypsin activation was analyzed in isolated acinar cells. Quantitative RT-PCR was used to examine the expression of pro-inflammatory mediators in the pancreas.
resultsPretreatment with trichostatin A decreased amylase levels by 70 % and protected against tissue injury in the pancreas. Moreover, HDAC inhibition reduced systemic IL-6 by more than 95 % and pulmonary myeloperoxidase activity by 75 %. Notably, inhibition of HDAC abolished taurocholate-induced gene expression of cyclooxygenase-2, MIP-2, monocyte chemotactic protein-1, IL-6, and IL-1β in the pancreas. In addition, HDAC inhibition reduced cerulein-induced trypsinogen activation in isolated acinar cells.
conclusionOur findings show that HDAC regulates trypsin activation, inflammation, and tissue damage in AP. Thus, targeting HDAC could serve as novel therapeutic approach in the management of severe AP.
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