Evidence map›Paper›PMID 27052008›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2016

K(+) channel blocker-induced neuroinflammatory response and neurological disorders: immunomodulatory effects of astaxanthin.

Nesrine Sifi, Marie-France Martin-Eauclaire, Fatima Laraba-Djebari

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

8 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Journal of microbiology and biotechnology · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Evaluation of neuroprotective effects of insulin on immuno-inflammatory and systemic disorders induced by kaliotoxin, a Kv1.3 channel blocker.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    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

3 authors at 3 institutions in 2 countries.

Nesrine SifiUSTHB, Faculty of Biological Sciences, Laboratory of Cellular and Molecular Biology, BP32, El Alia, Bab Ezzouar, 16111, Algiers, Algeria.
Marie-France Martin-EauclaireCRN2M UMR 7286, CNRS, Aix Marseille Université, 13344, Marseille Cedex 15, France.
Fatima Laraba-DjebariUSTHB, Faculty of Biological Sciences, Laboratory of Cellular and Molecular Biology, BP32, El Alia, Bab Ezzouar, 16111, Algiers, Algeria. flaraba@hotmail.com.
Aix-Marseille Université · FRUniversity of Algiers Benyoucef Benkhedda · DZUniversity of Sciences and Technology Houari Boumediene · DZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveChannelopathies due to the brain ion channel dysfunction is considered to be an important mechanism involved in various neurodegenerative diseases. In this study, we evaluated the ability of kaliotoxin (KTX) as K(+) channel blocker to induce neuro-inflammatory response and neurodegenerative alteration. We also investigate the effects of astaxanthin (ATX) against KTX disorders. MATERIAL AND TREATMENT: NMRI mice were injected with KTX (1 pg/kg, by i.c.v route) with or without pretreatment using ATX (80 mg/kg, o.p route).

resultsResults showed that KTX was detected in cerebral cortex area due to its binding to the specific receptors (immunofluorescence analysis). It induced an activation of inflammatory cascade characterized by an increase of IL-6, TNFα, NO, MDA levels and NF-κB expression associated to a decrease of GSH level. The neuroinflammatory response is accompanied with cerebral alterations and blood-brain barrier (BBB) disruption. The use of ATX prior to the KTX exerts a preventive effect not only on the neuroinflammation but also on altered tissues and the BBB disruption.

conclusionsKaliotoxin is able to induce neurological disorders by blocking the K(+) ion channel, and ATX suppresses this alterations with down regulation of IL-6, TNF-α and NF-κB expression in the brain.

Indexed as

AnimalsBrainCatalaseGlutathioneImmunologic FactorsInterleukin-6MalondialdehydeMiceNervous System DiseasesNF-kappa BNitric OxidePotassium Channel BlockersScorpion VenomsTumor Necrosis Factor-alphaXanthophyllsastaxanthineCatalaseGlutathioneImmunologic FactorsInterleukin-6interleukin-6, mousekaliotoxinMalondialdehydeNF-kappa BNitric OxidePotassium Channel BlockersScorpion VenomsTumor Necrosis Factor-alphaXanthophyllsAstaxanthinBlood–brain barrierK+ channel blockerNeurodegenerationNeuroinflammatory responseNeurotoxin

Identifiers

PMID27052008
OpenAlexW2320182043

What OpenQuestion holds

Textmetadata
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.