Evidence map›Paper›PMID 40200750›Full record

ArticleBrain and behavior2025

G-Protein-Coupled Receptor 84 Aggravates Early Brain Injury via Microglial NLRP3-ASC Inflammasome After Subarachnoid Hemorrhage.

Kun Jiang, Yan Zou, Yue Song, Long'jiang Zhou, Bing'tao Zhang, Xiao'ming Zhou, Xin Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain and behavior, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Kun JiangDepartment of Neurosurgery, Jinling Hospital, Jinling School of Clinical Medicine, Nanjing Medical University, Nanjing, China.
Yan ZouNanjing Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
Yue SongDepartment of Neurosurgery, Jinling Hospital, Jinling School of Clinical Medicine, Nanjing Medical University, Nanjing, China.
Long'jiang ZhouDepartment of Neurology, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, China.
Bing'tao ZhangNanjing Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
Xiao'ming ZhouNanjing Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
Xin ZhangDepartment of Neurosurgery, Jinling Hospital, Jinling School of Clinical Medicine, Nanjing Medical University, Nanjing, China.ORCID https://orcid.org/0000-0001-6822-3268

Funding

Jinling HospitalNational Natural Science Foundation of China 82071328
6 · The paper itself

Abstract

backgroundSubarachnoid hemorrhage (SAH) is one of the most devastating hemorrhagic strokes. SAH causes neuroinflammation and leads to both early brain injury and delayed brain injury. G-protein-coupled receptor 84 (GPR84), one of the orphan class-A G protein-coupled receptors (GPCRs), exerts pro-inflammatory and pro-phagocytic effects via targeting microglia in the central nervous system (CNS). This research investigated the role of GPR84 on SAH pathology via neuroinflammation.

methodsAn enzyme-linked immunosorbent assay was used for GPR84 expression in cerebrospinal fluid (CSF) samples from patients with SAH. An experimental SAH-model mouse was established by stereotactic injection of autologous blood into the chiasmatic cisterna. The SAH model in vitro was established by exposing microglia to hemoglobin. After inhibition of GPR84 in mice by GPR84-siRNA and GPR84-antagonist 3, the neurological deficits were evaluated by modified Garcia test, beam balance test, and Morris water maze. Neuronal death in SAH-model mice was evaluated by Nissl staining. GPR84, NLRP3 inflammasome, and cAMP/PKA expressions were detected by western blot and immunofluorescence.

resultsGPR84 was upregulated in patients after SAH onset. The GPR84 expression in microglia increased after SAH onset, activated NLRP3 inflammasome, and promoted IL-1β secretion. Both GPR84-shRNA and GPR84-antagonist 3 improved neurological deficits in SAH-model mice. Mechanistically, GPR84 activated the NLRP3 inflammasome via the cAMP/PKA signaling pathway to aggravate neuronal injury.

conclusionsGPR84 promotes NLRP3-mediated pyroptosis and activated NLRP3 inflammation via cAMP/PKA pathway.

Indexed as

Brain InjuriesInflammasomesMicrogliaNLR Family, Pyrin Domain-Containing 3 ProteinReceptors, G-Protein-CoupledSubarachnoid HemorrhageAdultAnimalsDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLMiddle AgedNeuroinflammatory DiseasesGpr84 protein, mouseInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanNlrp3 protein, mouseReceptors, G-Protein-CoupledG‐protein‐coupled receptor 84NLRP3 inflammasomepyroptosissubarachnoid hemorrhage

Identifiers

PMID40200750
PMCPMC11979352

What Socratic holds

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LicenceCC BY
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Registered trials

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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 Socratic graph.