Evidence map›Paper›PMID 36448290›Full record

ArticleBrain and behavior2023

Exercise postconditioning reduces ischemic injury via suppression of cerebral gluconeogenesis in rats.

Fengwu Li, Xiaokun Geng, Roxanne Ilagan, Shangying Bai, Yuhua Chen, Yuchuan Ding

Open access · goldAbstract read
In one paragraph

Article in Brain and behavior, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. The multifaceted impact of physical exercise on FoxO signaling pathways.Frontiers in cell and developmental biology · 2025
    Review
  4. Review
  5. Article
  6. Article
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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

6 authors at 3 institutions in 2 countries.

Fengwu LiChina-America Institute of Neuroscience, Beijing Luhe Hospital, Capital Medical University, Beijing, China.
Xiaokun GengChina-America Institute of Neuroscience, Beijing Luhe Hospital, Capital Medical University, Beijing, China.
Roxanne IlaganDepartment of Neurosurgery, Wayne State University School of Medicine, Detroit, Michigan, USA.
Shangying BaiChina-America Institute of Neuroscience, Beijing Luhe Hospital, Capital Medical University, Beijing, China.
Yuhua ChenDepartment of Developmental Cell Biology, Key Laboratory of Cell Biology, Ministry of Public Health, and Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, China.
Yuchuan DingDepartment of Neurosurgery, Wayne State University School of Medicine, Detroit, Michigan, USA.ORCID 0000-0001-8394-9147
Wayne State University · USMinistry of Education of the People's Republic of China · CNBeijing Luhe Hospital Affiliated to Capital Medical University · CN

Funding

National Natural Science Foundation of China 81802231National Natural Science Foundation of China 81871838National Natural Science Foundation of China 82002382the Science Foundation of Capital Medical University PYZ21170
6 · The paper itself

Abstract

Pre-stroke exercise conditioning reduces neurovascular injury and improves functional outcomes after stroke. The goal of this study was to explore if post-stroke exercise conditioning (PostE) reduced brain injury and whether it was associated with the regulation of gluconeogenesis. Adult rats received 2 h of middle cerebral artery (MCA) occlusion, followed by 24 h of reperfusion. Treadmill activity was then initiated 24 h after reperfusion for PostE. The severity of the brain damage was determined by infarct volume, apoptotic cell death, and neurological deficit at one and three days after reperfusion. We measured gluconeogenesis including oxaloacetate (OAA), phosphoenolpyruvate (PEP), pyruvic acid, lactate, ROS, and glucose via ELISA, as well as the location and expression of the key enzyme phosphoenolpyruvate carboxykinase (PCK)-1/2 via immunofluorescence. We also determined upstream pathways including forkhead transcription factor (FoxO1), p-FoxO1, 3-kinase (PI3K)/Akt, and p-PI3K/Akt via Western blot. Additionally, the cytoplasmic expression of p-FoxO1 was detected by immunofluorescence. Compared to non-exercise control, PostE (*p < .05) decreased brain infarct volumes, neurological deficits, and cell death at one and three days. PostE groups (*p < .05) saw increases in OAA and decreases in PEP, pyruvic acid, lactate, ROS, glucose levels, and tissue PCKs expression on both days. PCK-1/2 expressions were also significantly (*p < .05) suppressed by the exercise setting. Additionally, phosphorylated PI3K, AKT, and FoxO1 protein expression were significantly induced by PostE at one and three days (*p < .05). In this study, PostE reduced brain injury after stroke, in association with activated PI3K/AKT/FoxO1 signaling, and inhibited gluconeogenesis. These results suggest the involvement of FoxO1 regulation of gluconeogenesis underlying post-stroke neuroprotection.

Indexed as

Brain InjuriesStrokeAnimalsGluconeogenesisGlucoseInfarction, Middle Cerebral ArteryLactatesPhosphatidylinositol 3-KinasesPhosphoenolpyruvateProto-Oncogene Proteins c-aktPyruvic AcidRatsRats, Sprague-DawleyReactive Oxygen SpeciesGlucoseLactatesPhosphatidylinositol 3-KinasesPhosphoenolpyruvateProto-Oncogene Proteins c-aktPyruvic AcidReactive Oxygen SpeciesconditioninggluconeogenesisneuroprotectionPI3K/AKT/FoxO1rehabilitation

Identifiers

PMID36448290
PMCPMC9847623
OpenAlexW4310460642

What OpenQuestion 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 OpenQuestion graph.