Evidence map›Paper›PMID 30474696›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2019

Amitriptyline attenuates bleomycin-induced pulmonary fibrosis: modulation of the expression of NF-κβ, iNOS, and Nrf2.

Mai A Zaafan, Ahmed R Haridy, Amr M Abdelhamid

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 32 citations in OpenAlex.

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  13. p53 and Myofibroblast Apoptosis in Organ Fibrosis.International journal of molecular sciences · 2023
    Review
  14. Article
  15. Article
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  17. Pharmaceutics · 2021
    Article
  18. Article
  19. Article
  20. p53: A Key Protein That Regulates Pulmonary Fibrosis.Oxidative medicine and cellular longevity · 2020
    Review
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 1 institution in 1 country.

Mai A ZaafanPharmacology and Toxicology Department, Faculty of Pharmacy, October University for Modern Sciences and Arts (MSA), 6th of October, Egypt. makamel@msa.eun.eg.ORCID http://orcid.org/0000-0002-5295-0003
Ahmed R HaridyPharmacology and Toxicology Department, Faculty of Pharmacy, October University for Modern Sciences and Arts (MSA), 6th of October, Egypt.
Amr M AbdelhamidBiochemistry Department, Faculty of Pharmacy, October University for Modern Sciences and Arts (MSA), 6th of October, Egypt.
October University of Modern Sciences and Arts · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amitriptyline is a tricyclic antidepressant that was suggested to have antifibrotic potential. The current study aimed to investigate the modulatory effects of amitriptyline on bleomycin-induced pulmonary fibrosis in rats. Rats were randomly assigned into 4 groups: normal control, bleomycin control, amitriptyline+bleomycin, and amitriptyline only treated group. Lung injury was evaluated through the histological examination and immunohistochemical detection of α-smooth muscle actin (α-SMA) in lung tissue, in addition to the biochemical assessment of pulmonary contents of hydroxyproline and transforming growth factor beta-1 (TGF-β1). In addition, the following parameters were investigated for studying the possible mechanisms of amitriptyline antifibrotic effect: inducible nitric oxide synthase (iNOS), nuclear factor-κβ (NF-κβ), tumor necrosis factor-alpha (TNF-α), serpine-1, p53, nuclear factor erythroid 2-related factor 2 (Nrf2), lipid peroxides, and reduced glutathione (GSH). Amitriptyline exhibited potent antifibrotic effect that was reflected upon the histopathological examination and through its ability to suppress all the fibrotic parameters. Amitriptyline successfully suppressed the expression of NF-κβ, Nrf2, iNOS, and p53 in lung tissues besides the inhibition of other oxidative stress and inflammatory mediators. Amitriptyline could be a promising treatment to pulmonary fibrosis. Amitriptyline not only prevents the depression and its drawbacks in patients suffering from pulmonary fibrosis but also it can suppress fibrosis through variable mechanisms mainly via inhibition of NF-κβ/TNF-α/TGF-β pathway in addition to inhibition of Nrf2 and iNOS expression.

Indexed as

AmitriptylineAnimalsBleomycinLungMaleNF-E2-Related Factor 2NF-kappa BNitric Oxide Synthase Type IIPulmonary FibrosisRats, WistarAmitriptylineBleomycinNfe2l2 protein, ratNF-E2-Related Factor 2NF-kappa BNitric Oxide Synthase Type IINos2 protein, ratAmitriptylineiNOSNrf2Nuclear factor-κβPulmonary fibrosis

Identifiers

PMID30474696
OpenAlexW2900509955

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.