Evidence map›Paper›PMID 38409245›Full record

ArticleScientific reports2024

Sodium butyrate exerts a neuroprotective effect in rats with acute carbon monoxide poisoning by activating autophagy through the mTOR signaling pathway.

Jing Wen, Qiong Xu, Jing Li, Xuanyang Shen, Xiaolong Zhou, Jing Huang, Shiping Liu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. [Application of Animal Models in Research on Hypoxia-Related Diseases].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025
    Review
  3. Article
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 at 2 institutions in 1 country.

Jing WenDepartment of Emergency, Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, China.
Qiong XuDepartment of General Medicine, Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, China.
Jing LiDepartment of General Medicine, Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, China.
Xuanyang ShenDepartment of Emergency, Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, China.
Xiaolong ZhouDepartment of General Medicine, Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, China.
Jing HuangNorth Sichuan Medical College Innovation Center for Science and Technology, Nanchong, 637000, China.
Shiping LiuDepartment of General Medicine, Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, China. liusp456@163.com.
Affiliated Hospital of North Sichuan Medical College · CNNorth Sichuan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute carbon monoxide (CO) poisoning is a prevalent type of poisoning that causes significant harm globally. Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is a severe complication that occurs after acute CO poisoning; however, the exact underlying pathological cause of DEACMP remains unclear. Accumulating evidence indicates that abnormal inflammation and immune-mediated brain damage, cellular apoptosis and autophagy, and direct neuronal toxicity are involved in the development of delayed neurologic sequelae. Sodium butyrate, a histone deacetylase inhibitor, has gained increasing attention for its numerous beneficial effects on various diseases, such as obesity, diabetes, inflammatory diseases, and cerebral damage. In this study, an acute carbon monoxide poisoning (ACOP) model is established in rats to investigate the mechanism of CO poisoning and the therapeutic potential of sodium butyrate. The results suggested that the ACOP rats had impaired spatial memory, and cell apoptosis was observed in the hippocampi with activated autophagy. Sodium butyrate treatment further increased the activation of autophagy in the hippocampi of CO-exposed rats, inhibited apoptosis, and consolidated spatial memory. These findings indicated that sodium butyrate may improve memory and cognitive function in ACMP rats by promoting autophagy and inhibiting apoptosis.

Indexed as

Brain DiseasesBrain InjuriesCarbon Monoxide PoisoningNeuroprotective AgentsAnimalsAutophagyButyric AcidRatsSignal TransductionTOR Serine-Threonine KinasesButyric AcidmTOR protein, ratNeuroprotective AgentsTOR Serine-Threonine Kinases

Identifiers

PMID38409245
PMCPMC10897214
OpenAlexW4392164408

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.