Evidence map›Paper›PMID 39092643›Full record

ArticleCurrent neuropharmacology2024

Vitamin B6

Abdul Nasir, Mujeeb Ur Rahman, Manzar Khan, Muhammad Zahid, Muhammad Shahab, Hongjun Jiao, Amir Zeb, Shahid Ali Shah, Haroon Khan

Abstract read
In one paragraph

Article in Current neuropharmacology, 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. Review
  2. Article
  3. Review
  4. Association between serum vitamin BThe British journal of nutrition · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. 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

9 authors.

Abdul NasirMedical Research Center, Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Mujeeb Ur RahmanDepartment of Zoology, Islamia College Peshawar, Khyber Pakhtunkhwa, Pakistan.
Manzar KhanDepartment of Zoology, Hazara University Mansehra, Khyber Pakhtunkhwa, Pakistan.
Muhammad ZahidDepartment of Zoology, Islamia College Peshawar, Khyber Pakhtunkhwa, Pakistan.
Muhammad ShahabState Key Laboratories of Chemical Resources Engineering, Beijing University of Chemical Technology, Beijing 100029, PR China.
Hongjun JiaoDepartment of Pharmacy, Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Amir ZebDepartment of Natural and Basic Sciences, University of Turbat, Turbat 92600, Pakistan.
Shahid Ali ShahDepartment of Biology, University of Haripur, Khyber Pakhtunkhwa, Pakistan.
Haroon KhanDepartment of Pharmacy, Abdul Wali Khan University, Mardan, Khyber Pakhtunkhwa, Pakistan.

Funding

Science and Technology research project of Henan Provincial Department of Science and Technology 212102310315
6 · The paper itself

Abstract

backgroundCadmium chloride (Cd) is a pervasive environmental heavy metal pollutant linked to mitochondrial dysfunction, memory loss, and genetic disorders, particularly in the context of neurodegenerative diseases like Alzheimer's disease (AD).

methodsThis study investigated the neurotherapeutic potential of vitamin B6 (Vit. B6) in mitigating Cd-induced oxidative stress and neuroinflammation-mediated synaptic and memory dysfunction. Adult albino mice were divided into four groups: Control (saline-treated), Cd-treated, Cd+Vit. B6- treated, and Vit. B6 alone-treated. Cd and Vit. B6 were administered intraperitoneally, and behavioral tests (Morris Water Maze, Y-Maze) were conducted. Subsequently, western blotting, antioxidant assays, blood glucose, and hyperlipidemia assessments were performed.

resultsCd-treated mice exhibited impaired cognitive function, while Cd+Vit. B6-treated mice showed significant improvement. Cd-induced neurotoxic effects, including oxidative stress and neuroinflammation, were observed, along with disruptions in synaptic proteins (SYP and PSD95) and activation of p-JNK. Vit. B6 administration mitigated these effects, restoring synaptic and memory deficits. Molecular docking and MD simulation studies confirmed Vit. B6's inhibitory effect on IL-1β, NRF2, and p-JNK proteins.

conclusionThese results highlight Vit. B6 as a safe therapeutic supplement to mitigate neurodegenerative disorders, emphasizing the importance of assessing nutritional interventions for combating environmental neurotoxicity in the interest of public health.

Indexed as

Cadmium ChlorideHippocampusMemory DisordersNF-E2-Related Factor 2Oxidative StressVitamin B 6AnimalsAntioxidantsDisks Large Homolog 4 ProteinMaleMiceMolecular Docking SimulationNeuroinflammatory DiseasesNF-kappa BSignal TransductionSynaptophysinAntioxidantsCadmium ChlorideDisks Large Homolog 4 ProteinDlg4 protein, mouseNfe2l2 protein, mouseNF-E2-Related Factor 2NF-kappa BSynaptophysinSyp protein, mouseVitamin B 6Alzheimer's diseaseantiinflammatory.neurodegenerative diseaseneuroinflammationneurotoxicityOxidative stress

Identifiers

PMID39092643
PMCPMC11519820

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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.