ArticleScientific reports2023
Purinergic neurotransmission receptor P2X4 silencing alleviates intracerebral hemorrhage-induced neuroinflammation by blocking the NLRP1/Caspase-1 pathway.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- TIGAR overexpression alleviates intracerebral hemorrhage injury in mice by suppressing ATF4/NOX4/p22phox-mediated oxidative stress and inflammation.Acta pharmacologica Sinica · 2026Article
- AAV Vector-Mediated Modulation of Signaling Pathways in Neurological Disorders: Insights From Cellular, Animal, and Human Studies.Cell biochemistry and function · 2026Review
- Early peripheral blood gene expression predicts 90-day outcomes following subarachnoid hemorrhage.Journal of neuroinflammation · 2025Article
- Probenecid relieves LPS-induced neuroinflammation by modulating the NLRP1 inflammasome pathway in BV2 cells.Scientific reports · 2025Article
- Possible Interaction of Suramin with Thalamic P2X Receptors and NLRP3 Inflammasome Activation Alleviates Reserpine-Induced Fibromyalgia-Like Symptoms.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Hydrocephalus in primary brainstem hemorrhage risk predictors and management.Scientific reports · 2025Article
- Postoperative Serum NLRP1 as a Biochemical Predictor of Delirium and Cognitive Decline After Hip Fracture Surgery in Elderly Patients: A Single Center Observational Study.Clinical interventions in aging · 2025Observational
- 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
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study is performed to explore the role of P2X4 in intracerebral hemorrhage (ICH) and the association between P2X4 and the NLRP1/Caspase-1 pathway. The mouse ICH model was established via collagenase injection into the right basal ganglia. P2X4 expression in brain tissues was knocked down via intracerebroventricular injection with adeno-associated virus (AAV) harboring shRNA against shP2X4. The gene expression of P2X4 and protein levels related to NLRP1 inflammasome were detected using qRT-PCR and Western blot analysis, respectively. Muramyl dipeptide (an activator of NLRP1) was used to activate NLRP1 in brain tissues. ICH induced high expression of P2X4 in mouse brain tissues. The knockdown of P2X4 alleviated short- and long-term neurological deficits of ICH mice, as well as inhibited the tissue expression and serum levels of pro-inflammatory cytokines, including TNF-α, interleukin (IL)-6, and IL-1β. Additionally, the expressions of NLRP1, ASC, and pro-Caspase-1 were down-regulated upon P2X4 silencing. Moreover, neurological impairment and the expression and secretion of cytokines after P2X4 silencing were aggravated by the additional administration of MDP. P2X4 knockdown represses neuroinflammation in brain tissues after ICH. Mechanistically, P2X4 inhibition exerts a neuroprotective effect in ICH by blocking the NLRP1/Caspase-1 pathway.
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