Evidence map›Paper›PMID 28752628›Full record

ArticleClinical and experimental immunology2017

Intranasal delivery of dexamethasone efficiently controls LPS-induced murine neuroinflammation.

G Meneses, G Gevorkian, A Florentino, M A Bautista, A Espinosa, G Acero, G Díaz, A Fleury, I N Pérez Osorio, A Del Rey and 3 more

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 43 citations in OpenAlex.

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  15. Intranasal Dexamethasone Reduces Mortality and Brain Damage in a Mouse Experimental Ischemic Stroke Model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020
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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

13 authors at 2 institutions in 2 countries.

G MenesesInstituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, D.F., México.
G GevorkianInstituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, D.F., México.
A FlorentinoInstituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, D.F., México.
M A BautistaInstituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, D.F., México.
A EspinosaInstituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, D.F., México.
G AceroInstituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, D.F., México.
G DíazInstituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, D.F., México.
A FleuryUnidad Periférica del Instituto de Investigaciones Biomédicas en el Instituto Nacional de Neurología y Neurocirugía, México, D.F., México.
I N Pérez OsorioInstituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, D.F., México.
A Del ReyInstitute of Physiology and Pathophysiology, Medical Faculty, Philipps University, Marburg, Germany.
G FragosoInstituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, D.F., México.
E SciuttoInstituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, D.F., México.ORCID 0000-0001-5608-5355
H BesedovskyInstitute of Physiology and Pathophysiology, Medical Faculty, Philipps University, Marburg, Germany.
Universidad Nacional Autónoma de México · MXPhilipps University of Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroinflammation is the hallmark of several infectious and neurodegenerative diseases. Synthetic glucocorticoids (GCs) are the first-line immunosuppressive drugs used for controlling neuroinflammation. A delayed diffusion of GCs molecules and the high systemic doses required for brain-specific targeting lead to severe undesirable effects, particularly when lifelong treatment is required. Therefore, there is an urgent need for improving this current therapeutic approach. The intranasal (i.n.) route is being employed increasingly for drug delivery to the brain via the olfactory system. In this study, the i.n. route is compared to the intravenous (i.v.) administration of GCs with respect to their effectiveness in controlling neuroinflammation induced experimentally by systemic lipopolysaccharide (LPS) injection. A statistically significant reduction in interleukin (IL)-6 levels in the central nervous system (CNS) in the percentage of CD45

Indexed as

Cerebral CortexHippocampusMicrogliaNeurodegenerative DiseasesAdministration, IntranasalAnimalsAntigens, LyCalcium-Binding ProteinsCD11b AntigenGlial Fibrillary Acidic ProteinInterleukin-6Leukocyte Common AntigensLipopolysaccharidesMaleMiceMicrofilament ProteinsAif1 protein, mouseAntigens, LyCalcium-Binding ProteinsCD11b AntigenGlial Fibrillary Acidic Proteinglial fibrillary astrocytic protein, mouseInterleukin-6interleukin-6, mouseLeukocyte Common AntigensLipopolysaccharidesLy6G antigen, mouseMicrofilament Proteinsglucocorticoidsinflammationintranasal routeLPSneuroinflammation

Identifiers

PMID28752628
PMCPMC5680073
OpenAlexW2741954286

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.