Evidence map›Paper›PMID 42059927›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2026

Atomoxetine attenuates methotrexate-induced lung injury in rats implicating TLR4/NF-κB and Bax/Bcl-2/caspase-3 signaling cascades: a study based on molecular docking and experimental validation.

Reham H Mohyeldin, Ehab E Sharata, Ayman M Ibrahim, Mina Ezzat Attya, Al Shaimaa Mahmoud Kotb, Remon Roshdy Rofaeil, Yassmen Mohamed Montaser A Khalifa, Mahmoud Abdelnaser

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Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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.

Reham H MohyeldinDepartment of Pharmacology & Toxicology, Faculty of Pharmacy, Deraya University, 61111, Minia, Egypt.
Ehab E SharataDepartment of Pharmacology & Toxicology, Faculty of Pharmacy, Deraya University, 61111, Minia, Egypt.
Ayman M IbrahimDepartment of Pharmaceutical Chemistry, Faculty of Pharmacy, Deraya University, 61111, Minia, Egypt.
Mina Ezzat AttyaDepartment of Pathology, Faculty of Medicine, Minia University, Minia, 61519, Egypt.
Al Shaimaa Mahmoud KotbDepartment of Biochemistry, Molecular Biology and Physiology, Faculty of Medicine, Mutah University, Al‑Karak, Jordan.
Remon Roshdy RofaeilDepartment of Pharmacology & Toxicology, Faculty of Pharmacy, Deraya University, 61111, Minia, Egypt.
Yassmen Mohamed Montaser A KhalifaDepartment of Pharmacology & Toxicology, Faculty of Pharmacy, Deraya University, 61111, Minia, Egypt.
Mahmoud AbdelnaserDepartment of Biochemistry, Faculty of Pharmacy, Deraya University, 61111, Minia, Egypt. mahmoud.abdelnaser@deraya.edu.eg.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methotrexate (MTX) is frequently used to treat a variety of autoimmune diseases and malignancies, but its use is restricted due to a number of side effects, including lung damage. For the first time, this study attempts to assess the potential protective advantages of atomoxetine (ATOM) against MTX-induced lung damage in rats. MTX was used to cause lung damage. A total of 24 male Wistar albino rats were used in this study. Animals were randomly allocated to four experimental groups of six rats each: (Ⅰ) Control group, (Ⅱ) ATOM group, (Ⅲ) MTX group, and (Ⅳ) MTX+ATOM group. Malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD) levels in the lungs were measured. ELISA was used to measure the levels of lung IL-10, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), Bcl-2-associated X protein (Bax), and B-cell lymphoma 2 (Bcl-2). NF-κB p65 and caspase-3 were evaluated using immunohistochemistry. Toll-like receptor 4 (TLR4) and myeloid differentiation primary response 88 (MYD88) protein expression levels were assessed using the Western blot technique. A histopathological study of lung tissues was performed. Lung MDA, IL-6, TNF-α, and Bax levels were significantly increased by MTX, while GSH, SOD, IL-10, and Bcl-2 levels were significantly decreased. Additionally, this led to the overexpression of the proteins TLR4 and MYD88. Additionally, the MTX group had higher immunopositivity for both NF-κB p65 and caspase-3. All of the aforementioned biochemical and histological abnormalities were greatly improved with ATOM. ATOM significantly improved MTX-induced pulmonary injury by suppressing TLR4/MYD88/NF-κB p65 and caspase-3-mediated apoptotic signaling pathways.

Indexed as

Atomoxetine HydrochlorideLung InjuryMethotrexateAnimalsApoptosisbcl-2-Associated X ProteinCaspase 3LungMaleMolecular Docking SimulationNF-kappa BProto-Oncogene Proteins c-bcl-2RatsRats, WistarSignal TransductionToll-Like Receptor 4Atomoxetine HydrochlorideBax protein, ratbcl-2-Associated X ProteinBcl2 protein, ratCasp3 protein, ratCaspase 3MethotrexateNF-kappa BProto-Oncogene Proteins c-bcl-2Tlr4 protein, ratToll-Like Receptor 4AtomoxetineCaspase-3Lung injuryMethotrexateNF-κBTLR4

Identifiers

PMID42059927

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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.