Evidence map›Paper›PMID 26264367›Full record

ArticleBMC pulmonary medicine2015

Y-27632 is associated with corticosteroid-potentiated control of pulmonary remodeling and inflammation in guinea pigs with chronic allergic inflammation.

Patricia Angeli Pigati, Renato Fraga Righetti, Samantha Souza Possa, Beatriz Saraiva Romanholo, Adriana Palmeira Dias Rodrigues, Anelize Sartori Alves dos Santos, Débora Gonçalves Xisto, Mariana Alves Antunes, Carla Máximo Prado, Edna Aparecida Leick and 3 more

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 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
3.0field-weighted citation impact, top 9% 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, 38 citations in OpenAlex.

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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 3 institutions in 3 countries.

Patricia Angeli PigatiDepartment of Medicine, School of Medicine, University of São Paulo, São Paulo, Brazil. pangelipigati@gmail.com.
Renato Fraga RighettiDepartment of Medicine, School of Medicine, University of São Paulo, São Paulo, Brazil. renatofragar@yahoo.com.br.
Samantha Souza PossaDepartment of Medicine, School of Medicine, University of São Paulo, São Paulo, Brazil. samanthasz@hotmail.com.
Beatriz Saraiva RomanholoDepartment of Medicine, Laboratory of Experimental Therapeutics, LIM-20, School of Medicine, University of São Paulo, São Paulo, Brazil. beatrizmsaraiva@gmail.com.
Adriana Palmeira Dias RodriguesDepartment of Medicine, School of Medicine, University of São Paulo, São Paulo, Brazil. adrianapalmeira@hotmail.com.
Anelize Sartori Alves dos SantosDepartment of Medicine, School of Medicine, University of São Paulo, São Paulo, Brazil. anelize.sartori@hotmail.com.
Débora Gonçalves XistoLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Ilha do Fundão, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. deboraxisto@gmail.com.
Mariana Alves AntunesLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Ilha do Fundão, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. maryantunes@gmail.com.
Carla Máximo PradoDepartment of Medicine, School of Medicine, University of São Paulo, São Paulo, Brazil. cmaximoprado@gmail.com.
Edna Aparecida LeickDepartment of Medicine, School of Medicine, University of São Paulo, São Paulo, Brazil. leick51@yahoo.com.br.
Milton de Arruda MartinsDepartment of Medicine, School of Medicine, University of São Paulo, São Paulo, Brazil. mmartins@usp.br.
Patrícia Rieken Macedo RoccoLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Ilha do Fundão, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. prmrocco@gmail.com.
Iolanda de Fátima Lopes Calvo TibérioDepartment of Medicine, School of Medicine, University of São Paulo, São Paulo, Brazil. iocalvo@uol.com.br.
Universidade de São Paulo · BRCzech Academy of Sciences, Institute of Biophysics · CZYahoo (Spain) · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPreviously, we showed that treatment with the Rho-kinase inhibitor Y-27632 was able to control airway responsiveness, inflammation, remodeling, and oxidative stress in an animal model of asthma, suggesting that this drug is beneficial in asthma. However, studies evaluating the effects of these inhibitors in conjunction with corticosteroids on chronic pulmonary inflammation have not been conducted. Therefore, we evaluated the effects of treatment with the Rho-kinase inhibitor Y-27632, with or without concurrent dexamethasone treatment, on airway and lung tissue mechanical responses, inflammation, extracellular matrix remodeling, and oxidative stress in guinea pigs with chronic allergic inflammation.

methodsThe guinea pigs were subjected to seven ovalbumin or saline inhalation exposures. Treatment with Y-27632 (1 mM) and dexamethasone (2 mg/kg) started at the fifth inhalation. Seventy-two hours after the seventh inhalation, the pulmonary mechanics were evaluated and exhaled nitric oxide (ENO) levels were determined. The lungs were removed and histological analysis was performed using morphometry.

resultsThe treatment of guinea pigs with the Rho-kinase inhibitor and dexamethasone (ORC group) decreased ENO, the maximal mechanical responses after antigen challenge, inflammation, extracellular matrix remodeling and oxidative stress in the lungs. This therapeutic strategy reduced the levels of collagen and IFN-γ in the airway walls, as well as IL-2, IFN-γ, 8-iso-PGF2α and NF-κB in the distal parenchyma, when compared to isolated treatment with corticosteroid or Rho-kinase inhibitor (P < 0.05) and reduced the number of TIMP-1-positive cells and eosinophils in the alveolar septa compared to corticosteroid-treated animals (P < 0.05). The combined treatment with the Rho-kinase inhibitor and the corticosteroid provided maximal control over the remodeling response and inflammation in the airways and parenchyma.

conclusionsRho-kinase inhibition, alone or in combination with corticosteroids, can be considered a future pharmacological tool for the control of asthma.

Indexed as

Airway RemodelingAmidesAnimalsAsthmaChronic DiseaseDisease Models, AnimalDrug SynergismEnzyme InhibitorsGlucocorticoidsGuinea PigsInflammationLungPyridinesAmidesEnzyme InhibitorsGlucocorticoidsPyridinesY 27632

Identifiers

PMID26264367
PMCPMC4531528
OpenAlexW2107973823

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LicenceCC BY
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Registered trials

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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.