Evidence map›Paper›PMID 38472553›Full record

ArticleNeurochemical research2024

Remimazolam Attenuates LPS-Derived Cognitive Dysfunction via Subdiaphragmatic Vagus Nerve Target α7nAChR-Mediated Nrf2/HO-1 Signal Pathway.

Zhan Zhou, Ying Yang, Yi Wei, Yubo Xie

Open access · hybridAbstract read
In one paragraph

Article in Neurochemical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
9.7field-weighted citation impact, top 1% of its field
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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy.International journal of molecular sciences · 2026
    Review
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  19. Safety of Remimazolam in Vulnerable Populations.Drug design, development and therapy · 2025
    Review
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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

4 authors at 1 institution in 1 country.

Zhan Zhou *Department of Anesthesiology, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, China.
Ying Yang *Department of Anesthesiology, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, China.
Yi WeiDepartment of Anesthesiology, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, China.
Yubo XieDepartment of Anesthesiology, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, China. xybdoctor@163.com.ORCID http://orcid.org/0000-0002-7198-7506
Guangxi Medical University · CN

Funding

Guangxi Clinical Research Center for Anesthesiology No. GK AD22035214Special Fund of Neurotoxicity of General Anesthetics and Its Prevention and Treatment Innovation Team of the First Affiliated Hospital of Guangxi Medical University No. YYZS2022001the Key Project of Natural Science Foundation of Guangxi No. 2020GXNSFDA238025
6 · The paper itself

Abstract

Sepsis-induced neuroinflammation is significantly associated with sepsis-related brain dysfunction. Remimazolam is a novel ultra-short-acting benzodiazepine anesthetic with multiple organ protective effects. However, it is unknown whether remimazolam can ameliorate LPS-induced brain impairment. In this study, Lipopolysaccharide (5 mg/kg, LPS) severely impaired Sprague-Dawley rats spatial learning ability, memory, and cognitive function. However, remimazolam treatment showed a protective effect on LPS-induced cognitive dysfunction. Remimazolam partly reversed LPS-induced splenomegaly, decreased serum cytokine expression, suppressed hippocampal M1 microglial activation, and mitigated oxidative stress injury and neuroinflammation. Electroacupuncture (EA) or PNU282987 treatment improved LPS-induced cognitive dysfunction and also significantly inhibited neuroinflammation and systemic inflammation. However, MLA, ML385, or subdiaphragmatic vagus nerve (SDV) treatment abolished the protective effects of remimazolam. Further mechanistic studies showed that remimazolam induces protective effects by activating subdiaphragmatic vagus nerve target α7nAChR-mediated Nrf2/HO-1 signaling pathway. These results demonstrate that remimazolam can up-regulate α7nAChR, Cyto-Nrf2, HO-1, and cognitive-related (CREB, BDNF, PSD95) protein expressions, suppress M1 microglia, ameliorate neuroinflammation or systemic inflammation, and reverse cognitive dysfunction. Therefore, this study provides insight into a new therapeutic target for the treatment of sepsis-induced cerebral dysfunction.

Indexed as

Cognitive DysfunctionSepsisalpha7 Nicotinic Acetylcholine ReceptorAnimalsBenzodiazepinesInflammationLipopolysaccharidesNeuroinflammatory DiseasesNF-E2-Related Factor 2RatsRats, Sprague-DawleySignal TransductionVagus Nervealpha7 Nicotinic Acetylcholine ReceptorBenzodiazepinesLipopolysaccharidesNF-E2-Related Factor 2remimazolamCognitive dysfunctionLipopolysaccharideMicrogliaNeuroinflammationRemimazolam

Identifiers

PMID38472553
PMCPMC10991060
OpenAlexW4393953125

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.