ArticleBritish journal of pharmacology2016
Compound 9a, a novel synthetic histone deacetylase inhibitor, protects against septic injury in mice by suppressing MAPK signalling.
Article in British journal of pharmacology, 2016. 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, 29 citations in OpenAlex.
- Inhibition of Farnesoid-x-receptor signaling during abdominal sepsis by dysbiosis exacerbates gut barrier dysfunction.Cell communication and signaling : CCS · 2025Article
- Mechanism and application of feedback loops formed by mechanotransduction and histone modifications.Genes & diseases · 2024Review
- Gossypol improves myocardial dysfunction caused by sepsis by regulating histone acetylation.Clinical and translational science · 2023Article
- Acute respiratory distress syndrome heterogeneity and the septic ARDS subgroup.Frontiers in immunology · 2023Review
- Integrated Analysis Reveals the Potential Significance of HDAC Family Genes in Lung Adenocarcinoma.Frontiers in genetics · 2022Article
- The Surviving Sepsis Campaign: Basic/Translational Science Research Priorities.Critical care medicine · 2020Article
- The surviving sepsis campaign: basic/translational science research priorities.Intensive care medicine experimental · 2020Article
- Neuregulin‑1: An underlying protective force of cardiac dysfunction in sepsis (Review).Molecular medicine reports · 2020Review
- Metabolomics Coupled with Transcriptomics Approach Deciphering Age Relevance in Sepsis.Aging and disease · 2019Article
- Histone Deacetylation Inhibitors as Therapy Concept in Sepsis.International journal of molecular sciences · 2019Review
- Effects of FM0807, a novel curcumin derivative, on lipopolysaccharide-induced inflammatory factor release via the ROS/JNK/p53 pathway in RAW264.7 cells.Bioscience reports · 2018Article
- Ziziphus spina-christi leaf extract pretreatment inhibits liver and spleen injury in a mouse model of sepsis via anti-oxidant and anti-inflammatory effects.Inflammopharmacology · 2018Article
- Glutamine ameliorates lipopolysaccharide-induced cardiac dysfunction by regulating the toll-like receptor 4/mitogen-activated protein kinase/nuclear factor-kB signaling pathway.Experimental and therapeutic medicine · 2017Article
- Inhibition of epidermal growth factor receptor attenuates LPS-induced inflammation and acute lung injury in rats.Oncotarget · 2017Article
- Compound 9a, a novel synthetic histone deacetylase inhibitor, protects against septic injury in mice by suppressing MAPK signalling.British journal of pharmacology · 2016Article
- A novel imidazopyridine derivative, X22, attenuates sepsis-induced lung and liver injury by inhibiting the inflammatory response in vitro and in vivo.Drug design, development and therapy · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeSepsis is a life-threatening clinical condition characterized by uncontrolled inflammatory responses and is a major cause of death in intensive care units. Histone deacetylase (HDAC) inhibitors have recently exhibited anti-inflammatory properties. MAPK phosphatase (MKP) suppresses MAPK signalling, which plays an important role in inflammatory responses. The purpose of this study was to investigate the protective mechanisms of Compound 9a, a newly synthetized HDAC inhibitor, against septic injury. EXPERIMENTAL APPROACH: The anti-inflammatory properties of Compound 9a were assayed in LPS-stimulated RAW264.7 cells. In vivo, polymicrobial sepsis was induced in C57BL/6 mice by caecal ligation and puncture (CLP). The mice were treated with Compound 9a (i.p., 10 mg∙kg(-1) ) 2 h before and immediately after CLP. KEY
resultsCompound 9a inhibited the increased production of TNF-α, IL-6 and NO in LPS-stimulated RAW264.7 cells. In mice with CLP, Compound 9a improved survival rate, attenuated organ injuries and decreased serum TNF-α and IL-6 levels. CLP increased expression of toll-like receptor 4, phosphorylated (p)-p38, p-JNK and p-ERK proteins, which was attenuated by Compound 9a. Compound 9a decreased MKP-1 association with HDAC1 and enhanced MKP-1 acetylation and enhanced MKP-1 association with p-p38 and p-ERK. Moreover, the inhibitory effects of Compound 9a on serum cytokine levels and phosphorylation of MAPK were abolished by MKP-1 siRNA. CONCLUSIONS AND IMPLICATIONS: Our findings suggest that Compound 9a protected against septic injury by suppressing MAPK-mediated inflammatory signalling.
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