ArticleNeurochemical research2018
NLRP3 Inflammasome Is Involved in Q-VD-OPH Induced Necroptosis Following Cerebral Ischemia-Reperfusion Injury.
Article in Neurochemical research, 2018. 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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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- The Dual Roles of Microglia- and Astrocyte-Derived Exosomes in Cerebral Ischemia-Reperfusion Injury: from Intercellular Communication to Therapeutic Prospects.Molecular neurobiology · 2026Review
- Exploring potential biomarkers of NETosis-Related genes in spinal cord injury through machine learning and multi-omics analysis.Biochemistry and biophysics reports · 2026Article
- NLRP3-Mediated PANoptosis and Associated Interventions in Endothelial Injury.Cardiovascular toxicology · 2025Review
- PANoptosis: Cross-Talk Among Apoptosis, Necroptosis, and Pyroptosis in Neurological Disorders.Journal of inflammation research · 2025Review
- The Role of Necroptosis in Cerebral Ischemic Stroke.Molecular neurobiology · 2024Review
- New Insights on NLRP3 Inflammasome: Mechanisms of Activation, Inhibition, and Epigenetic Regulation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Review
- Cell Death Mechanisms in Cerebral Ischemia-Reperfusion Injury.Neurochemical research · 2022Review
- Nrf2 protects against cerebral ischemia-reperfusion injury by suppressing programmed necrosis and inflammatory signaling pathways.Annals of translational medicine · 2022Article
- A novel necroptosis-related lncRNA signature for predicting prognosis and anti-cancer treatment response in endometrial cancer.Frontiers in immunology · 2022Article
- Pan-caspase inhibition as a potential host-directed immunotherapy against MRSA and other bacterial skin infections.Science translational medicine · 2021Article
- Necroptosis: A Novel Pathway in Neuroinflammation.Frontiers in pharmacology · 2021Review
- Involvement of the miR-137-3p/CAPN-2 Interaction in Ischemia-Reperfusion-Induced Neuronal Apoptosis through Modulation of p35 Cleavage and Subsequent Caspase-8 Overactivation.Oxidative medicine and cellular longevity · 2020Article
- Pharmacological Inhibition of HDAC6 Attenuates NLRP3 Inflammatory Response and Protects Dopaminergic Neurons in Experimental Models of Parkinson's Disease.Frontiers in aging neuroscience · 2020Article
- Electroacupuncture Alleviates Ischemic Brain Injury by Inhibiting the miR-223/NLRP3 Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
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Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Necroptosis is a manner of caspase-independent cell death,which accounts for delayed ischemic cerebral injury, and can be used as a novel tool to expand the treatment time window in ischemic cerebral injury. Q-VD-OPH, a novel pan caspase inhibitor, has been identified as an inducer of necroptosis. In this study, we determined the optimal dose of Q-VD-OPH, which induces necroptosis in rats by the middle cerebral artery occlusion, followed by reperfusion. Furthermore, we report that the NLRP3 inflammasome is involved in necroptosis, with levels of NLRP3 inflammasome proteins as well as inflammatory cytokines, such as IL-1β, being elevated. We also demonstrated that NLRP3 was not only expressed in microglia and vascular endothelial cell, but also in neurons when necroptosis is induced with Q-VD-OPH. Inhibition of NLRP3 by glyburide strongly suppressed the expression of NLRP3 inflammasome proteins and IL-1β, and markedly reduced brain tissue damage. Our findings provide evidence that pretreatment with Q-VD-OPH suppresses apoptosis and induces necroptosis in the cerebral ischemia-reperfusion model. We also identified that the NLRP3 inflammasome plays an important role in neuronal necroptosis, and that NLRP3 inflammasome deficiency reduces brain tissue damage after cerebral ischemia-reperfusion injury in rats.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.