Evidence map›Paper›PMID 31113409›Full record

ArticleRespiratory research2019

Aminoguanidine affects systemic and lung inflammation induced by lipopolysaccharide in rats.

Saeideh Saadat, Farimah Beheshti, Vahid Reza Askari, Mahmoud Hosseini, Nema Mohamadian Roshan, Mohammad Hossein Boskabady

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-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

29 citing papers in PubMed, 58 citations in OpenAlex.

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  19. Mediators of inflammation · 2021
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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

6 authors at 2 institutions in 1 country.

Saeideh SaadatNeurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, 9177948564, Iran.
Farimah BeheshtiNeuroscience Research Center, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran.
Vahid Reza AskariNeurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, 9177948564, Iran.
Mahmoud HosseiniNeurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, 9177948564, Iran.
Nema Mohamadian RoshanDepartment of Pathology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Mohammad Hossein BoskabadyNeurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, 9177948564, Iran. boskabadymh@mums.ac.ir.
Mashhad University of Medical Sciences · IRTorbat Heydarieh University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNitric oxide is a mediator of potential importance in numerous physiological and inflammatory processes in the lung. Aminoguanidine (AG) has been shown to have anti-inflammation and radical scavenging properties. This study aimed to investigate the effects of AG, an iNOS inhibitor, on lipopolysaccharide (LPS)-induced systemic and lung inflammation in rats.

methodsMale Wistar rats were divided into control, LPS (1 mg/kg/day i.p.), and LPS groups treated with AG 50, 100 or 150 mg/kg/day i.p. for five weeks. Total nitrite concentration, total and differential white blood cells (WBC) count, oxidative stress markers, and the levels of IL-4, IFN-γ, TGF-β1, and PGE2 were assessed in the serum or bronchoalveolar lavage fluid (BALF).

resultsAdministration of LPS decreased IL-4 level (p < 0.01) in BALF, total thiol content, superoxide dismutase (SOD) and catalase (CAT) activities (p < 0.001) in BALF and serum, and increased total nitrite, malondialdehyde (MDA), IFN-γ, TGF-β1 and PGE2 (p < 0.001) concentrations in BALF. Pre-treatment with AG increased BALF level of IL-4 and total thiol as well as SOD and CAT activities (p < 0.05 to p < 0.001), but decreased BALF levels of total nitrite, MDA, IFN-γ, TGF-β1, and PGE2 (p < 0.01 to p < 0.001). AG treatment decreased total WBC count, lymphocytes and macrophages in BALF (p < 0.01 to p < 0.001) and improved lung pathological changes including interstitial inflammation and lymphoid infiltration (p < 0.05 to p < 0.001).

conclusionsAG treatment reduced oxidant markers, inflammatory cytokines and lung pathological changes but increased antioxidants and anti-inflammatory cytokines. Therefore, AG may play a significant protective role against inflammation and oxidative stress that cause lung injury.

Indexed as

AnimalsBronchoalveolar Lavage FluidDose-Response Relationship, DrugGuanidinesInflammation MediatorsLipopolysaccharidesMaleOxidative StressPneumoniaRandom AllocationRatsRats, WistarGuanidinesInflammation MediatorsLipopolysaccharidespimagedineAminoguanidineInflammationLipopolysaccharideLung injuryNitric oxide

Identifiers

PMID31113409
PMCPMC6530199
OpenAlexW2947388960

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LicenceCC BY
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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.