ArticleInflammation2015
Trichostatin A Protects Against Experimental Acute-on-Chronic Liver Failure in Rats Through Regulating the Acetylation of Nuclear Factor-κB.
Article in Inflammation, 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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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Identification and validation of integrated stress-response-related genes as biomarkers for age-related macular degeneration.Frontiers in molecular biosciences · 2025Article
- Prospect of Animal Models for Acute-on-chronic Liver Failure: A Mini-review.Journal of clinical and translational hepatology · 2022Review
- The Immune Pathogenesis of Acute-On-Chronic Liver Failure and the Danger Hypothesis.Frontiers in immunology · 2022Review
- Network pharmacology-based prediction of active compounds in the Wenyang Jiedu Huayu formula acting on acute-on-chronic liver failure with experimental supportFrontiers in pharmacology · 2022Article
- PPAR-γ Is Critical for HDAC3-Mediated Control of Oligodendrocyte Progenitor Cell Proliferation and Differentiation after Focal Demyelination.Molecular neurobiology · 2020Article
- FcεRI-HDAC3-MCP1 Signaling Axis Promotes Passive Anaphylaxis Mediated by Cellular Interactions.International journal of molecular sciences · 2019Review
- Modulations of Histone Deacetylase 2 Offer a Protective Effect through the Mitochondrial Apoptosis Pathway in Acute Liver Failure.Oxidative medicine and cellular longevity · 2019Article
- Quantitative Proteomic Analysis Reveals the Sites Related to Acetylation and Mechanism of ACY-1215 in Acute Liver Failure Mice.Frontiers in pharmacology · 2019Article
- Trichostatin A, a Histone Deacetylase Inhibitor, Alleviates Eosinophilic Meningitis Induced byFrontiers in microbiology · 2019Article
- The Protective Mechanism of CAY10683 on Intestinal Mucosal Barrier in Acute Liver Failure through LPS/TLR4/MyD88 Pathway.Mediators of inflammation · 2018Article
- Combined genetic and epigenetic interferences with interferon signaling expose prostate cancer cells to viral infection.Oncotarget · 2016Article
- Histone deacetylase 3 (HDAC 3) as emerging drug target in NF-κB-mediated inflammation.Current opinion in chemical biology · 2016Review
- HDAC 3-selective inhibitor RGFP966 demonstrates anti-inflammatory properties in RAW 264.7 macrophages and mouse precision-cut lung slices by attenuating NF-κB p65 transcriptional activity.Biochemical pharmacology · 2016Article
- Sustained Inhibition of Proliferative Response After Transient FGF Stimulation Is Mediated by Interleukin 1 Signaling.Journal of cellular physiology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase inhibitors (HDACi) were recently shown to suppress inflammatory responses in experimental models of autoimmune and inflammatory diseases. In this study, the protective effects of Trichostatin A (TSA), an HDACi, on experimental acute-on-chronic liver failure (ACLF) in rat were explored. An ACLF model was established in rats, and animals were randomly divided into control, model, and TSA-treated groups. The rats in TSA-treated group received TSA (2 mg/kg) at 2 h before induction of ACLF. Samples were obtained at 24 h after ACLF induction. We found that the rats in model group showed severe damage to liver tissue at 24 h after ACLF induction. TSA improved liver injury effectively. Serum tumor necrosis factor-alpha (TNF-α), interferon-γ (IFN-γ), interleukin (IL)-10, and IL-18 levels were significantly increased in model group compared with control group, but TSA reduced serum TNF-α, IFN-γ, IL-10, and IL-18 levels effectively compared with model group. In addition, TSA reduced the total HDAC activity, promoted the acetylation of histone, and decreased the expressions of class I HDAC in liver tissue. TSA also increased the acetylation levels and decreased phosphorylation levels in NF-κB p65. The median survival time of the rats was significantly prolonged in TSA-treated group. To conclude, TSA can inhibit the release of multiple inflammatory cytokines, prolong the survival time, and protect against ACLF in rats. The mechanisms were probably through enhancing the acetylation levels of non-histones rather than histone.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.