Evidence map›Paper›PMID 36926720›Full record

ArticleNeural regeneration research2023

Neuroprotective effects of meloxicam on transient brain ischemia in rats: the two faces of anti-inflammatory treatments.

Irene Fernández Ugidos, Paloma González-Rodríguez, María Santos-Galdiano, Enrique Font-Belmonte, Berta Anuncibay-Soto, Diego Pérez-Rodríguez, José Manuel Gonzalo-Orden, Arsenio Fernández-López

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. 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

8 authors at 3 institutions in 3 countries.

Irene Fernández UgidosÁrea de Biología Celular, Instituto de Biomedicina, Campus de Vegazana s/n, Universidad de León, León, Spain; Current address: Department of Pharmacology, Tulane University School of Medicine, New Orleans, LA, USA.
Paloma González-RodríguezÁrea de Biología Celular, Instituto de Biomedicina, Campus de Vegazana s/n, Universidad de León, León, Spain.
María Santos-GaldianoÁrea de Biología Celular, Instituto de Biomedicina, Campus de Vegazana s/n, Universidad de León, León; Neural Therapies SL. Edif. Institutos de Investigación. Planta baja. Local B43. Campus de Vegazana s/n. León, Spain.
Enrique Font-BelmonteÁrea de Biología Celular, Instituto de Biomedicina, Campus de Vegazana s/n, Universidad de León, León, Spain; Current address: Department of Neurology, David Geffen School of Medicine at University of California (UCLA), Los Angeles, CA, USA.
Berta Anuncibay-SotoÁrea de Biología Celular, Instituto de Biomedicina, Campus de Vegazana s/n, Universidad de León, León, Spain; Current address: Department of Life Sciences, Imperial College London (ICL), London, UK.
Diego Pérez-RodríguezÁrea de Biología Celular, Instituto de Biomedicina, Campus de Vegazana s/n, Universidad de León, León, Spain; Current address: Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, London, UK.
José Manuel Gonzalo-OrdenÁrea de Biología Celular, Instituto de Biomedicina, Campus de Vegazana s/n, Universidad de León; Department of Medicina, Cirugía y Anatomía Veterinaria, University of León, León, Spain.
Arsenio Fernández-LópezÁrea de Biología Celular, Instituto de Biomedicina, Campus de Vegazana s/n, Universidad de León, León, Spain; Current address: Department of Pharmacology, Tulane University School of Medicine, New Orleans, LA, USA.
Universidad de León · ESTulane University · USUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The inflammatory response plays an important role in neuroprotection and regeneration after ischemic insult. The use of non-steroidal anti-inflammatory drugs has been a matter of debate as to whether they have beneficial or detrimental effects. In this context, the effects of the anti-inflammatory agent meloxicam have been scarcely documented after stroke, but its ability to inhibit both cyclooxygenase isoforms (1 and 2) could be a promising strategy to modulate post-ischemic inflammation. This study analyzed the effect of meloxicam in a transient focal cerebral ischemia model in rats, measuring its neuroprotective effect after 48 hours and 7 days of reperfusion and the effects of the treatment on the glial scar and regenerative events such as the generation of new progenitors in the subventricular zone and axonal sprouting at the edge of the damaged area. We show that meloxicam's neuroprotective effects remained after 7 days of reperfusion even if its administration was restricted to the two first days after ischemia. Moreover, meloxicam treatment modulated glial scar reactivity, which matched with an increase in axonal sprouting. However, this treatment decreased the formation of neuronal progenitor cells. This study discusses the dual role of anti-inflammatory treatments after stroke and encourages the careful analysis of both the neuroprotective and the regenerative effects in preclinical studies.

Indexed as

anti-inflammatoriesastrocyteaxonal sproutingcylinder testdoublecortinfocal brain ischemiaglial scarinflammationneuroprotectionnew neuron generationtransient stroke

Identifiers

PMID36926720
PMCPMC10233777
OpenAlexW4317629395

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.