Evidence map›Paper›PMID 42426909›Full record

ArticleBehavioral and brain functions : BBF2026

Microglia-specific NLRP3 inhibition mitigates hippocampal neuroinflammation and cognitive deficits after hemorrhagic shock with resuscitation.

Ya-Mei Zhang, Meng-Yue Wang, Zhong-Yong Zhang, Xin-Yu Yang, Hong-Lian Duan, Jian-Kai Sun, Xiao-Yi Ma, Rong-Xin Song, Jing-Yu Hui, Dong-Xue Zhang and 2 more

Abstract read
In one paragraph

Article in Behavioral and brain functions : BBF, 2026. 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

12 authors.

Ya-Mei Zhang *Department of Anesthesiology, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou, China.
Meng-Yue Wang *Graduate School, Hebei University of Chinese Medicine, Shijiazhuang, China.
Zhong-Yong ZhangDepartment of Endocrinology, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou, China.
Xin-Yu YangCangzhou Central Blood Station, Cangzhou, China.
Hong-Lian DuanGraduate School, Hebei University of Chinese Medicine, Shijiazhuang, China.
Jian-Kai SunGraduated School, Hebei Medical University, Shijiazhuang, China.
Xiao-Yi MaGraduate School, Hebei University of Chinese Medicine, Shijiazhuang, China.
Rong-Xin SongDepartment of Anesthesiology, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou, China.
Jing-Yu HuiGraduated School, Hebei North University, Zhangjiakou, China.
Dong-Xue ZhangDepartment of Gerontology, Cangzhou Central Hospital, Cangzhou, China.
Li-Min ZhangDepartment of Anesthesiology, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou, China.
Hui-Tao MiaoDepartment of Anesthesiology, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou, China. m2418513532@163.com.ORCID http://orcid.org/0000-0001-5550-3885

Funding

National Natural Science Foundation of Cangzhou 221001011DNational Natural Science Foundation of China 81701296Natural Science Foundation of Hebei Province H2021110004Natural Science Foundation of Hebei Province H2024110009
6 · The paper itself

Abstract

backgroundCognitive dysfunction is a prevalent mental health problem following hemorrhagic shock with resuscitation (HSR). Our previous work indicated that neuroinflammation caused by nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), which is modulated by glial cells, such as microglia, is potentially significant in developing emotional and cognitive dysfunction. However, little is known about the potential of microglial NLRP3 to treat HSR-induced cognitive dysfunction. Therefore, this study established an HSR rodent model to investigate whether microglial NLRP3 represents a potential therapeutic target for improving cognitive dysfunction after HSR.

methodsAn HSR model was developed by inducing bleeding and retransfusion in mice. The Morris water maze and Novel object recognition tests were used for behavioral evaluation. To selectively knock out the NLRP3 inflammasome in microglia, the AAV‑CX3CR1‑Cre (pAAV‑CX3CR1‑NLS‑Cre‑P2A‑EGFP‑3xFLAG‑WPRE) virus was stereotaxically injected into the hippocampal CA1 region of male C57BL/6 mice with NLRP3

resultsOur findings indicated that the NLRP3 inhibitor MCC950 significantly reversed HSR-induced lower recognition index, increased escape latency, reduced platform crossings, decreased θ and γ power and θ-γ phase coupling, decreased intensity of PSD95 and Synaptophysin, increased number of Iba1

conclusionOur study demonstrates that inhibition of microglia‑specific NLRP3 can mitigate cognitive impairment following HSR, identifying microglial NLRP3 as a promising therapeutic target. This effect may be associated with suppressing pyroptosis via the NLRP3 signaling pathway in microglia.

Indexed as

Cognitive DysfunctionHippocampusMicrogliaNeuroinflammatory DiseasesNLR Family, Pyrin Domain-Containing 3 ProteinShock, HemorrhagicAnimalsDisease Models, AnimalFuransHeterocyclic Compounds, 4 or More RingsIndenesInflammasomesMaleMiceMice, Inbred C57BLMice, KnockoutFuransHeterocyclic Compounds, 4 or More RingsIndenesInflammasomesN-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamideNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseSulfonamidesSulfonesCognitive dysfunctionHemorrhagic shock with resuscitationInflammationMicrogliaNLRP3

Identifiers

PMID42426909
PMCPMC13563706

What OpenQuestion holds

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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 OpenQuestion graph.