Evidence map›Paper›PMID 26109901›Full record

ArticleInterdisciplinary toxicology2014

Modulation of microglial function by the antidepressant drug venlafaxine.

Michal Dubovický, Eszter Császár, Kristína Melicherčíková, Marcela Kuniaková, Lucia Račková

Open access · diamondAbstract read
In one paragraph

Article in Interdisciplinary toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 32% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. The role of microglia in neuropsychiatric disorders and suicide.European archives of psychiatry and clinical neuroscience · 2022
    Review
  3. Modulation of microglial activation by antidepressants.Journal of psychopharmacology (Oxford, England) · 2022
    Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
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  10. 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

5 authors at 3 institutions in 2 countries.

Michal DubovickýInstitute of Experimental Pharmacology & Toxicology, Slovak Academy of Sciences, Department of Developmental and Behavioral Toxicology, Bratislava, Slovakia.
Eszter CsászárInstitute of Experimental Pharmacology & Toxicology, Slovak Academy of Sciences, Department of Developmental and Behavioral Toxicology, Bratislava, Slovakia.
Kristína MelicherčíkováInstitute of Experimental Pharmacology & Toxicology, Slovak Academy of Sciences, Department of Developmental and Behavioral Toxicology, Bratislava, Slovakia.
Marcela KuniakováInstitute of Medical Biology, Genetics and Clinical Genetics, Faculty of Medicine, Comenius University in Bratislava, Bratislava, Slovak Republic.
Lucia RačkováInstitute of Experimental Pharmacology & Toxicology, Slovak Academy of Sciences, Department of Developmental and Behavioral Toxicology, Bratislava, Slovakia.
Institute of Experimental Pharmacology and Toxicology of the Slovak Academy of Sciences · SKComenius University Bratislava · SKSlovak Academy of Sciences · SK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An increasing amount of data suggests that depression is an inflammatory disease. Depressed patients have higher peripheral blood levels of inflammatory markers which have been shown to access the brain and interact with the pathophysiological domain known to be involved in depression. Furthermore, microglia activation may play an important role in the inflammatory pathophysiology of depression. In BV-2 microglia cell line, the present study investigated the potential anti-inflammatory effects of venlafaxine, along with its potential influence on injury of lipopolysaccharide (LPS)-stimulated cells. Although venlafaxine showed only marginal influence on the majority of the pro-inflammatory parameters assessed (in particular NO release, phagocytosis and proliferation), it significantly suppressed superoxide production by the stimulated cells. In addition, venlafaxine exerted also a protective effect on mitochondrial membrane potential and lysosomes of the stimulated microglia. In conclusion, our results suggest that although VEN might have only a marginal effect on major pro-inflammatory parameters of microglia, its inhibitory effect on superoxide generation can contribute to the prevention of harmful effects of oxidative and nitrosative stress involved in the pathogenesis of depression. Moreover, the protective effect of VEN on viability of microglia can prevent a rapid reduction of these cells, thus avoiding limitations of several physiological processes in the brain and possibly also the progression of depression.

Indexed as

cytoprotectiondepressioninflammationmicrogliavenlafaxine

Identifiers

PMID26109901
PMCPMC4436209
OpenAlexW2042016989

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.