ArticleJournal of molecular neuroscience : MN2017
NLRP3 is Required for Complement-Mediated Caspase-1 and IL-1beta Activation in ICH.
Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 72 citations in OpenAlex.
- The Interaction of Neutrophil Extracellular Traps and Complement in Intracerebral Hemorrhage.Cellular and molecular neurobiology · 2026Review
- Rhein Inhibits NLRP3 Activation and Alleviates Microglial Pyroptosis After Intracerebral Hemorrhage in Rats.Brain and behavior · 2026Article
- Article
- Targeting the NLRP3-ROS Axis: Disrupting the Oxidative-Inflammatory Vicious Cycle in Intracerebral Hemorrhage.Journal of inflammation research · 2025Review
- A new perspective on the regulation of neuroinflammation in intracerebral hemorrhage: mechanisms of NLRP3 inflammasome activation and therapeutic strategies.Frontiers in immunology · 2025Review
- Prognostic Significance of Serum NLRP3 in Spontaneous Intracerebral Hemorrhage.International journal of general medicine · 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
- FERM domain containing kindlin 1 knockdown attenuates inflammation induced by intracerebral hemorrhage in rats via NLR family pyrin domain containing 3/nuclear factor kappa B pathway.Experimental animals · 2023Article
- Oxymatrine ameliorates white matter injury by modulating gut microbiota after intracerebral hemorrhage in mice.CNS neuroscience & therapeutics · 2023Article
- The Potential of NLRP3 Inflammasome as a Therapeutic Target in Neurological Diseases.Molecular neurobiology · 2023Review
- A20 ameliorates disc degeneration by suppressing mTOR/BNIP3 axis-mediated mitophagy.Genes & genomics · 2023Article
- Exosomal miR-23b from bone marrow mesenchymal stem cells alleviates oxidative stress and pyroptosis after intracerebral hemorrhage.Neural regeneration research · 2023Article
- Secondary White Matter Injury Mediated by Neuroinflammation after Intracerebral Hemorrhage and Promising Therapeutic Strategies of Targeting the NLRP3 Inflammasome.Current neuropharmacology · 2023Review
- High plasma complement C4 levels as a novel predictor of clinical outcome in intracerebral hemorrhage.Frontiers in aging neuroscience · 2023Article
- Ferrostatin-1 Polarizes Microglial Cells Toward M2 Phenotype to Alleviate Inflammation After Intracerebral Hemorrhage.Neurocritical care · 2022Article
- Granulocyte colony-stimulating factor protected against brain injury in a rat cerebral hemorrhage model by modulating inflammation.Experimental animals · 2022Article
- Mechanisms of neuroinflammation in hydrocephalus after intraventricular hemorrhage: a review.Fluids and barriers of the CNS · 2022Review
- Perspectives on the mechanism of pyroptosis after intracerebral hemorrhage.Frontiers in immunology · 2022Review
- Caspase-1: A Promising Target for Preserving Blood-Brain Barrier Integrity in Acute Stroke.Frontiers in molecular neuroscience · 2022Review
- Microglial pyroptosis: Therapeutic target in secondary brain injury following intracerebral hemorrhage.Frontiers in cellular neuroscience · 2022Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complement-mediated inflammation plays a vital role in intracerebral hemorrhage (ICH), implicating pro-inflammatory factor interleukin-1beta (IL-1β) secretion. Brain samples and contralateral hemiencephalon were all collected and detected by Western blot. NLRP3 expression was located by dual immunofluorescence staining at 1, 3, and 5 days post-ICH. Brain water content was examined post-ICH. The neural deficit scores were evaluated by observers blindly. ILs were detected by ELISA. SiRNAs targeting NLRP3 (siNLRP3), siASC, and siControl were injected to inhibit NLRP3 function. To test the complement activation via Nod-like receptor (NLR) family pyrin domain-containing 3 (NLRP3), normal rabbit complement (NRC) was injected with lipopolysaccharide (LPS) to facilitate the complement function. As a result, complement 3a (C3a) and complement 5a (C5a) were upregulated during the ICH-induced neuroinflammation, and ablation of C3 attenuates ICH-induced IL-1β release. Though the LPS rescues the neuroinflammation in the ICH model, C3 deficiency attenuates the LPS-induced inflammatory effect. The NLRP3 inflammasome was activated after ICH and was located in the microglial cell of the mouse brain, which exhibits a time-dependent manner. However, the number of NLRP3/Iba-1 dual-labeled cells in the C3
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