ArticleJournal of neuroinflammation2023
HMGB1 mediates synaptic loss and cognitive impairment in an animal model of sepsis-associated encephalopathy.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 114 citations in OpenAlex.
- Early amyloid pathology in mice synergistically worsens post-sepsis behavioral impairment and microglial synaptic phagocytosis.Brain, behavior, & immunity - health · 2026Article
- HMGB1 in Amyloid-Beta Pathology: Mechanistic Insights and Therapeutic Implications for Alzheimer's Disease.International journal of molecular sciences · 2026Review
- Glial-neuronal crosstalk via GABA signaling: mechanistic insights into neuropsychiatric and neurological pathophysiology.Molecular psychiatry · 2026Review
- Protein-protein interaction-mediated signaling networks in ischemic stroke: from molecular mechanisms to therapeutic strategies.Acta pharmacologica Sinica · 2026Review
- Hydrogen alleviates sepsis-associated encephalopathy via ATG9B-dependent mitophagy.Molecular medicine (Cambridge, Mass.) · 2026Article
- Microglia and neuroinflammation: function, heterogeneity, and crosstalk.Cellular & molecular immunology · 2026Review
- Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy.International journal of molecular sciences · 2026Review
- Microglial Activation Mediates Drp1-Dependent Mitochondrial Fission and Neuronal Apoptosis in a Lipopolysaccharide-Induced Model of Cognitive Dysfunction.Molecular neurobiology · 2026Article
- Microglial galectin-3 disrupts parvalbumin interneurons and hippocampal synchrony, driving cognitive deficits.Journal of neuroinflammation · 2026Article
- Emerging biomodels to understand the pathophysiology of sepsis and evaluate new therapeutic strategies targeting extracellular histones.Materials today. Bio · 2026Review
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- Microglia-Mediated Dysfunction of PKCγ Interneurons Underlies the Mechanical Hypersensitivity in Autism.Molecular neurobiology · 2026Article
- Recombinant Human Thymosin β4 Attenuates Endotoxemia-Induced ALI and EAE by Suppressing Inflammatory and Oxidative Responses.Biomolecules · 2026Article
- State-dependent neuronal and network dynamics in the lateral hypothalamus across sevoflurane anesthesia-emergence revealed by microelectrode arrays.Microsystems & nanoengineering · 2026Article
- Inflachromene Blocks Neuronal HMGB1 Translocation to Mitigate Hippocampal TLR4-NF-κB-Mediated Neuroinflammation and Depression-Like Behavior After Spinal Cord Injury.Molecular neurobiology · 2026Article
- Clostridium butyricum ameliorates Toxoplasma gondii-induced neuropsychiatric disorders by attenuating glial-mediated synaptic pruning via the gut-brain axis.Journal of neuroinflammation · 2026Article
- Hypothalamic arcuate microglia in sepsis: AgRP circuit engagement and ARHGAP24-dependent remodeling.Journal of neuroinflammation · 2026Article
- A genomic structural equation modelling study elucidates shared genetic architecture of polygenic traits associated with post-intensive care syndrome.Scientific reports · 2026Article
- Tiaobu Xinshen Recipe Improves Cognitive Deficits by Alleviating Synaptic Ultrastructure Degradation and Reducing Amyloid β in Transgenic Mice of Alzheimer's Disease.Chinese journal of integrative medicine · 2026Article
- CAR Treg therapies for neurodegenerative diseases.iScience · 2026Review
10 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundMicroglial activation-mediated neuroinflammation is one of the essential pathogenic mechanisms of sepsis-associated encephalopathy (SAE). Mounting evidence suggests that high mobility group box-1 protein (HMGB1) plays a pivotal role in neuroinflammation and SAE, yet the mechanism by which HMGB1 induces cognitive impairment in SAE remains unclear. Therefore, this study aimed to investigate the mechanism of HMGB1 underlying cognitive impairment in SAE.
methodsAn SAE model was established by cecal ligation and puncture (CLP); animals in the sham group underwent cecum exposure alone without ligation and perforation. Mice in the inflachromene (ICM) group were continuously injected with ICM intraperitoneally at a daily dose of 10 mg/kg for 9 days starting 1 h before the CLP operation. The open field, novel object recognition, and Y maze tests were performed on days 14-18 after surgery to assess locomotor activity and cognitive function. HMGB1 secretion, the state of microglia, and neuronal activity were measured by immunofluorescence. Golgi staining was performed to detect changes in neuronal morphology and dendritic spine density. In vitro electrophysiology was performed to detect changes in long-term potentiation (LTP) in the CA1 of the hippocampus. In vivo electrophysiology was performed to detect the changes in neural oscillation of the hippocampus.
resultsCLP-induced cognitive impairment was accompanied by increased HMGB1 secretion and microglial activation. The phagocytic capacity of microglia was enhanced, resulting in aberrant pruning of excitatory synapses in the hippocampus. The loss of excitatory synapses reduced neuronal activity, impaired LTP, and decreased theta oscillation in the hippocampus. Inhibiting HMGB1 secretion by ICM treatment reversed these changes.
conclusionsHMGB1 induces microglial activation, aberrant synaptic pruning, and neuron dysfunction in an animal model of SAE, leading to cognitive impairment. These results suggest that HMGB1 might be a target for SAE treatment.
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