ArticleOxidative medicine and cellular longevity2022
Inhibiting Microglia-Derived NLRP3 Alleviates Subependymal Edema and Cognitive Dysfunction in Posthemorrhagic Hydrocephalus after Intracerebral Hemorrhage via AMPK/Beclin-1 Pathway.
Article in Oxidative medicine and cellular longevity, 2022. 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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16 citing papers in PubMed, 22 citations in OpenAlex.
- Liposomal curcumin nanocarrier ameliorates synaptic dysfunction after intracerebral hemorrhage.Inflammopharmacology · 2026Article
- Delayed microglial depletion protects against white matter injury following neonatal cerebral hemorrhage in mice.Neural regeneration research · 2026Article
- The neurobiological regulatory mechanism of brain edema.Frontiers in cellular neuroscience · 2026Review
- Article
- Feasibility Study on Inflammasome Proteins as Biomarkers in the Cerebrospinal Fluid of Pediatric Patients with Hydrocephalus Due to Intraventricular Hemorrhage.Biomolecules · 2025Article
- Cannabinoid Receptors Reduced Early Brain Damage by Regulating NOX-2 and the NLRP3 Inflammasome in an Animal Model of Intracerebral Hemorrhage.CNS neuroscience & therapeutics · 2025Article
- Diagnostic value of serum NLRP3, metalloproteinase-9 and interferon-γ for postoperative hydrocephalus and intracranial infection in patients with severe craniocerebral trauma.Experimental physiology · 2024Article
- NLRP3 Inflammasome Inhibitors for Antiepileptogenic Drug Discovery and Development.International journal of molecular sciences · 2024Review
- TXNIP/NLRP3 aggravates global cerebral ischemia-reperfusion injury-induced cognitive decline in mice.Heliyon · 2024Article
- Review
- Neutrophil extracellular trap-mediated impairment of meningeal lymphatic drainage exacerbates secondary hydrocephalus after intraventricular hemorrhage.Theranostics · 2024Article
- Spi1 regulates the microglial/macrophage inflammatory response via the PI3K/AKT/mTOR signaling pathway after intracerebral hemorrhage.Neural regeneration research · 2024Article
- Oxymatrine ameliorates white matter injury by modulating gut microbiota after intracerebral hemorrhage in mice.CNS neuroscience & therapeutics · 2023Article
- Role of α-synuclein in microglia: autophagy and phagocytosis balance neuroinflammation in Parkinson's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Cannabinoid receptor-2 attenuates neuroinflammation by promoting autophagy-mediated degradation of the NLRP3 inflammasome post spinal cord injury.Frontiers in immunology · 2022Article
- Autophagy regulates inflammation in intracerebral hemorrhage: Enemy or friend?Frontiers in cellular neuroscience · 2022Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For posthemorrhagic hydrocephalus (PHH) patients, whether occur subependymal edema indicates poor outcomes, partially manifested as cognitive impairment. In the brain, NLRP3 inflammasome mainly derived from microglia/macrophages is involved in proinflammatory and neurodeficits after hemorrhage, and autophagy is vital for neuronal homeostasis and functions. Accumulating evidence suggest that NLRP3 inflammasome and autophagy played an essential role after intracerebral hemorrhage (ICH). We aimed to dissect the mechanisms underlying subependymal edema formation and cognitive dysfunction. Here, based on the hydrocephalus secondary to ICH break into ventricular (ICH-IVH) in rats, this study investigated whether microglia/macrophage-derived NLRP3 induced subependymal edema formation and neuron apoptosis in subventricular zones (SVZ). In the acute phase of ICH-IVH, both the expression of NLRP3 inflammasome of microglia/macrophages and the autophagy of neurons were upregulated. The activated NLRP3 in microglia/macrophages promoted the release of IL-1beta to extracellular, which contributed to excessive autophagy, leading to neurons apoptosis both in vivo and in vitro through the AMPK/Beclin-1 pathway combined with transcriptomics. Administration of MCC950 (NLRP3 inflammasome specific inhibitor) after ICH-IVH significantly reduced edema formation and improved cognitive dysfunction. Thus, inhibiting NLRP3 activation in SVZ may be a promising therapeutic strategy for PHH patients that warrants further investigation.
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