Evidence map›Paper›PMID 40724875›Full record

ArticleInternational journal of molecular sciences2025

Thiamine Compounds Alleviate Oxidative Stress, Over-Expression of Pro-Inflammatory Markers and Behavioral Abnormalities in a Mouse Predation Model of PTSD.

Tatyana Strekalova, Anna Gorlova, Joao Costa-Nunes, Aleksandr Litavrin, Johannes P M de Munter, Alexei Lyundup, Aleksei Umriukhin, Andrey Proshin, Allan V Kalueff, Edna Grünblatt and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

11 authors.

Tatyana StrekalovaDepartment of Psychiatry and Neuropsychology, Maastricht University, 6211 LK Maastricht, The Netherlands.
Anna GorlovaResearch and Education Resource Center, Peoples Friendship University of Russia (RUDN University), 117198 Moscow, Russia.
Joao Costa-NunesFaculdade de Medicina, Universidade de Lisboa, Campo Grande, 1649-028 Lisboa, Portugal.ORCID 0000-0003-0127-5420
Aleksandr LitavrinDepartment of Normal Physiology, Sechenov University, 119048 Moscow, Russia.ORCID 0009-0004-0460-4992
Johannes P M de MunterDepartment of Psychiatry and Neuropsychology, Maastricht University, 6211 LK Maastricht, The Netherlands.ORCID 0000-0001-7583-1464
Alexei LyundupResearch and Education Resource Center, Peoples Friendship University of Russia (RUDN University), 117198 Moscow, Russia.
Aleksei UmriukhinDepartment of Normal Physiology, Sechenov University, 119048 Moscow, Russia.
Andrey ProshinLaboratory of Cognitive Psychophysiology, Federal Research Center for Innovator and Emerging Biomedical and Pharmaceutical Technologies, 125315 Moscow, Russia.ORCID 0000-0002-7258-7870
Allan V KalueffSuzhou Municipal Key Laboratory of Neurobiology and Cell Signaling, Department of Biosciences and Bioinformatics, School of Science, Xi'an Jiaotong-Liverpool University, Suzhou 215123, China.
Edna GrünblattDepartment of Child and Adolescent Psychiatry and Psychotherapy, University of Zurich, 8032 Zurich, Switzerland.ORCID 0000-0001-8505-7265
Susanna WalitzaDepartment of Child and Adolescent Psychiatry and Psychotherapy, University of Zurich, 8032 Zurich, Switzerland.

Funding

European Union's HORIZON 2020 research and innovation program 101007642Research Russia-Switzerland Grant-2020 RRSW-2020
6 · The paper itself

Abstract

Experiences of life-threatening stimuli can induce post-traumatic stress disorder (PTSD), which is associated with long-lasting behavioral and neurochemical abnormalities. Despite its increased global incidence, the current treatment options for PTSD remain limited, highlighting the need for novel therapeutic strategies. As oxidative stress and neuroinflammation contribute to PTSD, the use of powerful antioxidants such as thiamine (B1 vitamin) compounds may counteract disease development. Young C57BL/6 mice received thiamine or benfotiamine in drinking water (each at a dose of 200 mg/kg/day) for 21 days, and for the last five days, they were subjected to rat exposure. Mice were studied for anxiety-like behavior, exploration, locomotion, grooming, social interactions, pain sensitivity, brain changes in protein carbonyl (PC), total glutathione (TG), and gene expression of distress and inflammation markers. Rat exposure induced anxiety-like behavior, excessive grooming, and alteration in locomotion, along with other abnormalities. Stressed, untreated mice had elevated levels of PC and TG in the prefrontal cortex, hippocampus, amygdala, and striatum and increased expression of

Indexed as

Behavior, AnimalOxidative StressStress Disorders, Post-TraumaticThiamineAnimalsAntioxidantsAnxietyBiomarkersBrainDisease Models, AnimalInflammationMaleMiceMice, Inbred C57BLRatsAntioxidantsbenphothiamineBiomarkersThiamineanimal modelanxiety-like behaviorbenfotiaminemiceneuroinflammationoxidative stressposttraumatic stress disorder (PTSD)predator stressthiamine (vitamin B1)

Identifiers

PMID40724875
PMCPMC12294334

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.