Evidence map›Paper›PMID 39692820›Full record

ArticleMolecular neurobiology2025

Acute Treatment with Fucoidan Ameliorates Traumatic Brain Injury-Induced Neurological Damages and Memory Deficits in Rats: Role of BBB Integrity, Microglial Activity, Neuroinflammation, and Oxidative Stress.

Shahla Eyvari-Brooshghalan, Rasool Haddadi, Siamak Shahidi, Shahab Ghaderi, Masome Rashno, Ali Kalantari, Iraj Salehi, Alireza Komaki, Abdolrahman Sarihi

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Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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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

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Shahla Eyvari-BrooshghalanDepartment of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamedan, Iran.
Rasool HaddadiDepartment of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamedan, Iran.
Siamak ShahidiDepartment of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamedan, Iran.
Shahab GhaderiDepartment of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamedan, Iran.
Masome RashnoAsadabad School of Medical Sciences, Asadabad, Iran.
Ali KalantariDepartment of Pathobiology, Faculty of Veterinary Medicine, Bu-Ali Sina University, Hamedan, Iran.
Iraj SalehiNeurophysiology Research Center, Hamadan University of Medical Sciences, Hamedan, Iran.
Alireza KomakiDepartment of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamedan, Iran. alirezakomaki@gmail.com.
Abdolrahman SarihiDepartment of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamedan, Iran. arahmansarihi@gmail.com.

Funding

Vice Chancellor for Research and Technology, Hamadan University of Medical Sciences 1401121611052
6 · The paper itself

Abstract

There is no acquiesced remedy for the treatment of traumatic brain injury (TBI)-associated impairment, especially cognitive decline. The first 24 h after TBI is a golden time for preventing the progress of the impairments. The present study aimed to examine the acute effects of fucoidan on neurological outcomes and memory performance and investigate its potential mechanisms in rats with TBI. Fucoidan (25, 50, and 100 mg/kg, i.p.) was injected immediately after TBI induction. Veterinary coma scale (VCS), brain edema, blood-brain barrier (BBB) integrity, passive avoidance memory and spatial memory, neuroplasticity, myeloperoxidase (MPO) activity, oxidative stress, and histological alteration were evaluated after TBI induction and fucoidan treatment. The findings revealed that TBI resulted in an enhancement in brain water content and BBB permeability and diminished the performance of passive avoidance memory and spatial memory. These were accompanied by long-term potentiation (LTP) suppression in the hippocampus and the prevention of activities of SOD, catalase, and GPx and enhancement of MPO activity, TNF-α, IL-6, and lipid peroxidation levels in the hippocampus as well as hippocampal neuronal loss. Fascinatingly, acute treatment of TBI rats with fucoidan especially in the higher doses (50 and 100 mg/kg) significantly ameliorated (p < 0.05) neurological outcomes of VCS, cerebral edema, BBB integrity, passive avoidance memory, spatial memory, LTP impairment, and oxidative-antioxidative balance. Also, fucoidan significantly ameliorated hippocampal neuronal loss, TNF-α and IL-6 levels, and MPO activity as an indicator of microglial activation. These outcomes imply that fucoidan can be a hopeful remedy for TBI-associated neuronal impairments. However, further research is necessary to endorse this issue.

Indexed as

Blood-Brain BarrierBrain Injuries, TraumaticMemory DisordersMicrogliaNeuroinflammatory DiseasesOxidative StressPolysaccharidesAnimalsBrain EdemaHippocampusMaleNeuroprotective AgentsRatsRats, WistarSpatial MemoryfucoidanNeuroprotective AgentsPolysaccharidesFucoidanLong-term potentiation (LTP)MemoryMPO activityOxidative stressTraumatic brain injury

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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 Socratic graph.