ArticleMolecular neurobiology2020
NLRP3 Activation Contributes to Acute Brain Damage Leading to Memory Impairment in Sepsis-Surviving Rats.
Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- The Key Drivers of Brain Injury by Systemic Inflammatory Responses after Sepsis: Microglia and Neuroinflammation.Molecular neurobiology · 2023Pooled it
- NLRP3 inflammasome: A link between systemic infection and Alzheimer's disease.Neural regeneration research · 2026Article
- Impact of Chronic Mild Stress on Neurotrophic and Hypothalamic-Pituitary-Adrenal Factors in the Brain of Rats Submitted to Sepsis.Neurotoxicity research · 2026Article
- The P2X7 receptor/NLRP3 inflammasome signaling axis in sepsis: molecular mechanisms, organ-specific pathophysiology, and emerging therapeutic strategies.Purinergic signalling · 2026Review
- Hyperbaric oxygen therapy in sepsis-associated encephalopathy: pathophysiological rationale, preclinical evidence, and translational challenges.Frontiers in cellular neuroscience · 2026Review
- The role of microglia in sepsis-associated encephalopathy: a narrative review.Translational pediatrics · 2025Review
- Exploring NLRP3 Inhibition as a Key Modulator in Neonatal Hypoxic-Ischemic Brain Injury.Neuromolecular medicine · 2025Review
- Effect of subclinical esketamine on NLRP3 and cognitive dysfunction in elderly ischemic stroke patients.Open medicine (Warsaw, Poland) · 2025Article
- Article
- Targeting glycolysis for neuroprotection in early LPS-induced neuroinflammation.Brain, behavior, & immunity - health · 2024Article
- Oxidative stress and mitochondrial dysfunction contributes to postoperative cognitive dysfunction in elderly rats dependent on NLRP3 activation.Metabolic brain disease · 2024Article
- Targeted rescue of synaptic plasticity improves cognitive decline in sepsis-associated encephalopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Inflammasomes in neurological disorders - mechanisms and therapeutic potential.Nature reviews. Neurology · 2024Review
- "Brain Fog" After COVID-19 Infection: How the Field of Neuropsychology Can Help Clear the Air.Advances in experimental medicine and biology · 2024Article
- NLRP3 Activation Contributes to Memory Impairment in an Experimental Model of Pneumococcal Meningitis.Molecular neurobiology · 2024Article
- Amelioration of Neurochemical Alteration and Memory and Depressive Behavior in Sepsis by Allopurinol, a Tryptophan 2,3-Dioxygenase Inhibitor.CNS & neurological disorders drug targets · 2024Article
- Mechanism of baixiangdan capsules on anti-neuroinflammation: combining dry and wet experiments.Aging · 2023Article
- Neurochemical effects of sepsis on the brain.Clinical science (London, England : 1979) · 2023Article
- NLRP3 Inflammasome's Activation in Acute and Chronic Brain Diseases-An Update on Pathogenetic Mechanisms and Therapeutic Perspectives with Respect to Other Inflammasomes.Biomedicines · 2023Review
- Methods to Study Inflammasome Activation in the Central Nervous System: Immunoblotting and Immunohistochemistry.Methods in molecular biology (Clifton, N.J.) · 2023Article
Corrections and comments
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Authors and funding
22 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis survivors present acute and long-term cognitive impairment and the pathophysiology of neurological dysfunction in sepsis involves microglial activation. Recently, the involvement of cytosolic receptors capable of forming protein complexes called inflammasomes have been demonstrated to perpetuate neuroinflammation. Thus, we investigated the involvement of the NLRP3 inflammasome activation on early and late brain changes in experimental sepsis. Two-month-old male Wistar rats were submitted to the sepsis model by cecal ligation and perforation (CLP group) or laparotomy only (sham group). Immediately after surgery, the animals received saline or NLRP3 inflammasome formation inhibitor (MCC950, 140 ng/kg) intracerebroventricularly. Prefrontal cortex and hippocampus were isolated for cytokine analysis, microglial and astrocyte activation, oxidative stress measurements, nitric oxide formation, and mitochondrial respiratory chain activity at 24 h after CLP. A subset of animals was followed for 10 days for survival assessment, and then behavioral tests were performed. The administration of MCC950 restored the elevation of IL-1β, TNF-α, IL-6, and IL-10 cytokine levels in the hippocampus. NLRP3 receptor levels increased in the prefrontal cortex and hippocampus at 24 h after sepsis, associated with microglial, but not astrocyte, activation. MCC950 reduced oxidative damage to lipids and proteins as well as preserved the activity of the enzyme SOD in the hippocampus. Mitochondrial respiratory chain activity presented variations in both structures studied. MCC950 reduced microglial activation, decreased acute neurochemical and behavioral alteration, and increased survival after experimental sepsis.
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