Evidence map›Paper›PMID 26388737›Full record

ArticleFrontiers in cellular neuroscience2015

Benfotiamine upregulates antioxidative system in activated BV-2 microglia cells.

Iva Bozic, Danijela Savic, Ivana Stevanovic, Sanja Pekovic, Nadezda Nedeljkovic, Irena Lavrnja

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

6 authors at 3 institutions in 1 country.

Iva BozicInstitute for Biological Research "Siniša Stanković," University of Belgrade Belgrade, Serbia.
Danijela SavicInstitute for Biological Research "Siniša Stanković," University of Belgrade Belgrade, Serbia.
Ivana StevanovicInstitute for Medical Research, Military Medical Academy Belgrade, Serbia.
Sanja PekovicInstitute for Biological Research "Siniša Stanković," University of Belgrade Belgrade, Serbia.
Nadezda NedeljkovicFaculty of Biology, Institute for Physiology and Biochemistry, University of Belgrade Belgrade, Serbia.
Irena LavrnjaInstitute for Biological Research "Siniša Stanković," University of Belgrade Belgrade, Serbia.
Institute for Biological Research “Siniša Stanković”Institute of General and Physical Chemistry · RSMilitary Medical Academy · RS

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic microglial activation and resulting sustained neuroinflammatory reaction are generally associated with neurodegeneration. Activated microglia acquires proinflammatory cellular profile that generates oxidative burst. Their persistent activation exacerbates inflammation, which damages healthy neurons via cytotoxic mediators, such as superoxide radical anion and nitric oxide. In our recent study, we have shown that benfotiamine (S-benzoylthiamine O-monophosphate) possesses anti-inflammatory effects. Here, the effects of benfotiamine on the pro-oxidative component of activity of LPS-stimulated BV-2 cells were investigated. The activation of microglia was accompanied by upregulation of intracellular antioxidative defense, which was further promoted in the presence of benfotiamine. Namely, activated microglia exposed to non-cytotoxic doses of benfotiamine showed increased levels and activities of hydrogen peroxide- and superoxide-removing enzymes-catalase and glutathione system, and superoxide dismutase. In addition, benfotiamine showed the capacity to directly scavenge superoxide radical anion. As a consequence, benfotiamine suppressed the activation of microglia and provoked a decrease in NO and (·)O(-) 2 production and lipid peroxidation. In conclusion, benfotiamine might silence pro-oxidative activity of microglia to alleviate/prevent oxidative damage of neighboring CNS cells.

Indexed as

benfotiaminecatalaseglutathioneLPSmicrogliaoxidative stress

Identifiers

PMID26388737
PMCPMC4559599
OpenAlexW1650915434

What OpenQuestion 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 OpenQuestion graph.