Evidence map›Paper›PMID 38715815›Full record

ArticleAmerican journal of translational research2024

Semaglutide alleviates early brain injury following subarachnoid hemorrhage by suppressing ferroptosis and neuroinflammation via SIRT1 pathway.

Lei Chen, Haiting Xu, Chunlei Zhang, Jianqing He, Yuhai Wang

Abstract read
In one paragraph

Article in American journal of translational research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Shikonin attenuates blood-brain barrier injury and oxidative stress in rats with subarachnoid hemorrhage by activating Sirt1/Nrf2/HO-1 signaling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  10. Potential role of SIRT1 in cell ferroptosis.Frontiers in cell and developmental biology · 2025
    Review
  11. Article
  12. Spotlight on the Mechanism of Action of Semaglutide.Current issues in molecular biology · 2024
    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

5 authors.

Lei ChenDepartment of Neurosurgery, The Fifth Clinical Medical College of Anhui Medical University Hefei, Anhui, China.
Haiting XuDepartment of Emergency, Joint Logistics Support Unit No. 904 Hospital Wuxi, Jiangsu, China.
Chunlei ZhangDepartment of Neurosurgery, The Fifth Clinical Medical College of Anhui Medical University Hefei, Anhui, China.
Jianqing HeDepartment of Neurosurgery, The Fifth Clinical Medical College of Anhui Medical University Hefei, Anhui, China.
Yuhai WangDepartment of Neurosurgery, The Fifth Clinical Medical College of Anhui Medical University Hefei, Anhui, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesSubarachnoid hemorrhage (SAH) is a major cause of incapacity and death, imposing a significant economic burden globally. Additionally, SAH is the third most prevalent form of stroke. Semaglutide affects oxidative stress, inflammation, and mitochondrial biogenesis. Specifically, the potential neuroprotective effect of semaglutide in SAH and its underlying mechanism is unclear. Accordingly, the present research intended to explore the neuroprotective effect of semaglutide in SAH and its potential molecular mechanisms.

methodsWe constructed a C57BL/6 mouse model of SAH. The parameters assessed were neuronal ferroptosis, neuroinflammatory cytokine levels, reactive oxygen species (ROS) levels, glutathione (GSH) and malondialdehyde (MDA) levels, brain water content, and neurological score.

resultsThe results showed that the activation of semaglutide significantly increased neurological scores, relieved cerebral edema, decreased the levels of inflammatory cytokine nuclear factor kappa B, interleukin (IL)-1β, IL-6, tumor necrosis factor-alpha, MDA, and ROS, and increased the levels of GSH. Suppression of SIRT1 reversed these effects, indicating that semaglutide activated SIRT1 to reduce neuroinflammation, ferroptosis, and neuronal cell death after SAH. Thus, the activation of the Nrf2/HO-1 signaling pathway contributes to the neuroprotective properties of semaglutide.

conclusionsSemaglutide can improve murine neurological outcomes and reduce neuronal damage against neuroinflammation and ferroptosis.

Indexed as

early brain injuryFerroptosisneuroinflammationSAHSIRT1

Identifiers

PMID38715815
PMCPMC11070367

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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.