Evidence map›Paper›PMID 38136154›Full record

ArticleAntioxidants (Basel, Switzerland)2023

Hyperbaric Oxygen Therapy Alleviates Memory and Motor Impairments Following Traumatic Brain Injury via the Modulation of Mitochondrial-Dysfunction-Induced Neuronal Apoptosis in Rats.

Reem Sakas, Katya Dan, Doron Edelman, Saher Abu-Ata, Aviv Ben-Menashe, Yaseen Awad-Igbaria, Jean Francois-Soustiel, Eilam Palzur

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 18 citations in OpenAlex.

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  8. Mitochondria transfer in tissue homeostasis and diseases.International journal of biological sciences · 2026
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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

8 authors at 3 institutions in 1 country.

Reem SakasAzrieli Faculty of Medicine, Bar-Ilan University, Safed 1311502, Israel.
Katya DanAzrieli Faculty of Medicine, Bar-Ilan University, Safed 1311502, Israel.
Doron EdelmanNeurosurgery Department, Tel-Aviv Sourasky Medical Center, Tel-Aviv 6423906, Israel.
Saher Abu-AtaAzrieli Faculty of Medicine, Bar-Ilan University, Safed 1311502, Israel.
Aviv Ben-MenasheAzrieli Faculty of Medicine, Bar-Ilan University, Safed 1311502, Israel.
Yaseen Awad-IgbariaAzrieli Faculty of Medicine, Bar-Ilan University, Safed 1311502, Israel.
Jean Francois-SoustielAzrieli Faculty of Medicine, Bar-Ilan University, Safed 1311502, Israel.
Eilam PalzurResearch Institute of Galilee Medical Center, Nahariya 221001, Israel.ORCID 0000-0003-2032-2974
Bar-Ilan University · ILTel Aviv Sourasky Medical Center · ILWestern Galilee Hospital · IL

Funding

Medical Corps Ministry of Defense in Israel Research No.014453
6 · The paper itself

Abstract

Traumatic brain injury (TBI) is a leading cause of morbidity and mortality in young adults, characterized by primary and secondary injury. Primary injury is the immediate mechanical damage, while secondary injury results from delayed neuronal death, often linked to mitochondrial damage accumulation. Hyperbaric oxygen therapy (HBOT) has been proposed as a potential treatment for modulating secondary post-traumatic neuronal death. However, the specific molecular mechanism by which HBOT modulates secondary brain damage through mitochondrial protection remains unclear. Spatial learning, reference memory, and motor performance were measured in rats before and after Controlled Cortical Impact (CCI) injury. The HBOT (2.5 ATA) was performed 4 h following the CCI and twice daily (12 h intervals) for four consecutive days. Mitochondrial functions were assessed via high-resolution respirometry on day 5 following CCI. Moreover, IHC was performed at the end of the experiment to evaluate cortical apoptosis, neuronal survival, and glial activation. The current result indicates that HBOT exhibits a multi-level neuroprotective effect. Thus, we found that HBOT prevents cortical neuronal loss, reduces the apoptosis marker (cleaved-Caspase3), and modulates glial cell proliferation. Furthermore, HBO treatment prevents the reduction in mitochondrial respiration, including non-phosphorylation state, oxidative phosphorylation, and electron transfer capacity. Additionally, a superior motor and spatial learning performance level was observed in the CCI group treated with HBO compared to the CCI group. In conclusion, our findings demonstrate that HBOT during the critical period following the TBI improves cognitive and motor damage via regulating glial proliferation apoptosis and protecting mitochondrial function, consequently preventing cortex neuronal loss.

Indexed as

apoptosishyperbaric oxygen therapy (HBOT)mitochondria respirationsecondary brain injurytraumatic brain injury

Identifiers

PMID38136154
PMCPMC10740762
OpenAlexW4388943810

What Socratic 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 Socratic graph.