ArticleExperimental & molecular medicine2021
The pivotal role of the NLRC4 inflammasome in neuroinflammation after intracerebral hemorrhage in rats.
Article in Experimental & molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- Targeted plasma proteomics reveals a central role of upregulated TNFRSF proteins in HIV-associated stroke.Nature communications · 2026Article
- Glucose-responsive "sense-and-treat" microneedle patch for promoting diabetic chronic wound healing.Materials today. Bio · 2026Article
- Neuronal inflammasomes: balancing immunity, neuroinflammation, and homeostasis.Trends in immunology · 2026Review
- Mitophagy Inhibition Suppresses Seizures in Status Epilepticus Mice by Decreasing Hippocampal NLRC4 Expression.Journal of molecular neuroscience : MN · 2026Article
- Immunoregulatory mechanisms in parasitic eosinophilic lung disease: the role of IgE immune complexes and NLRC4 inflammasome.Frontiers in immunology · 2026Review
- Chrysin Improves Cognitive Dysfunction in Rats with Intracerebral Hemorrhage by Regulating the Nrf2/GPX4 Pathway to Inhibit Ferroptosis.Molecular neurobiology · 2025Article
- Targeting pyroptosis in myocardial inflammation and fibrosis: molecular mechanisms and therapeutic strategies.Apoptosis : an international journal on programmed cell death · 2025Review
- Overexpression of Heme Oxygenase 1 Enhances the Neuroprotective Effects of Exosomes in Subarachnoid Hemorrhage by Suppressing Oxidative Stress and Endoplasmic Reticulum Stress.Molecular neurobiology · 2025Article
- Review
- G Protein-Coupled Receptor 30 Attenuates Neuronal Pyroptosis Induced by Subarachnoid Hemorrhage.Mediators of inflammation · 2025Article
- Astrocyte-microglia crosstalk in subarachnoid hemorrhage: mechanisms and treatments.Frontiers in immunology · 2025Review
- Interleukin-1 Receptor-Associated Kinase-3 Aggravates Neuroinflammatory Injury After Intracerebral Hemorrhage via Activation NF-κB/IL-17A Pathway in Mice.Journal of inflammation research · 2025Article
- Cystatin C Attenuates Perihematomal Secondary Brain Injury by Inhibiting the Cathepsin B/NLRP3 Signaling Pathway in a Rat Model of Intracerebral Hemorrhage.Molecular neurobiology · 2024Article
- A Prospective Cohort Study of Elevated Serum NLRP1 Levels to Prognosticate Neurological Outcome After Acute Intracerebral Hemorrhage at a Single Academic Institution.Neuropsychiatric disease and treatment · 2024Article
- Genetics of Primary Hemophagocytic Lymphohistiocytosis.Advances in experimental medicine and biology · 2024Review
- The Role of Histone Deacetylases in NLRP3 Inflammasomesmediated Epilepsy.Current molecular medicine · 2024Review
- 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
- Prognostic significance of serum NLRC4 in patients with acute supratentorial intracerebral hemorrhage: A prospective longitudinal cohort study.Frontiers in neurology · 2023Article
- Ferroptosis: Underlying mechanism and the crosstalk with other modes of neuronal death after intracerebral hemorrhage.Frontiers in cellular neuroscience · 2023Review
- Evaluation of Serum NLRC4 as a Potential Prognostic Biochemical Marker in Humans with Severe Traumatic Brain Injury: A Prospective Cohort Study.Risk management and healthcare policy · 2023Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NLRC4 inflammasome, a member of the nucleotide-binding and oligomerization domain-like receptor (NLR) family, amplifies inflammation by facilitating the processing of caspase-1, interleukin (IL)-1β, and IL-18. We explored whether NLRC4 knockdown alleviated inflammatory injury following intracerebral hemorrhage (ICH). Furthermore, we investigated whether NLRC4 inflammasome activation can be adjusted by the regulator of G protein signaling 2/leucine-rich repeat kinase-2 pathway. Fifty microliters of arterial blood was drawn and injected into the basal ganglion to simulate the ICH model. NLRC4 small interfering RNAs (siRNAs) were utilized to knockdown NLRC4. An LRRK2 inhibitor (GNE7915) was injected into the abdominal cavity. Short hairpin (sh) RNA lentiviruses and lentiviruses containing RGS2 were designed and applied to knockdown and promote RGS2 expression. Neurological functions, brain edema, Western blot, enzyme-linked immunosorbent, hematoxylin and eosin staining, Nissl staining, immunoprecipitation, immunofluorescence assay and Evans blue dye extravasation and autofluorescence assay were evaluated. It was shown that the NLRC4 inflammasome was activated following ICH injury. NLRC4 knockdown extenuated neuronal death, damage to the blood-brain barrier, brain edema and neurological deficiency 3 days after ICH. NLRC4 knockdown reduced myeloperoxidase (MPO) cells as well as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β and IL-18 following ICH. GNE7915 reduced pNLRC4 and NLRC4 inflammasome activation. RGS2 suppressed the interaction of LRRK2 and NLRC4 and NLRC4 inflammasome activation by regulating pLRRK2. Our study demonstrated that the NLRC4 inflammasome may aggravate the inflammatory injury induced by ICH and that RGS2/LRRK2 may relieve inflammatory injury by restraining NLRC4 inflammasome activation.
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