ArticleMolecular biology reports2026
Naringenin attenuates amiodarone-induced pulmonary fibrosis in rats via modulation of the SIRT1/NF-κB signalling pathway.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAmiodarone (AMD)-induced pulmonary fibrosis (PF) is a serious adverse effect driven by oxidative stress and inflammation. Naringenin [NAR], a citrus flavonoid, possesses potent antioxidant and anti-inflammatory properties. This study investigated the protective effects of NAR against AMD-induced PF in rats, focusing on the sirtuin 1; nuclear factor Kappa -B (SIRT1/NF-κB) pathway.
methodsThirty-two male Wistar rats were divided into four experimental groups (n = 8): control (CON), (NAR), (AMD), and AMD + NAR. In the AMD groups, PF was induced using AMD. NAR treatment was administered daily via oral gavage for five weeks.
resultsAfter 5 weeks, the AMD group exhibited significant alveolar damage and collagen deposition. Biochemically, AMD induced severe oxidative stress, characterized by increased malondialdehyde and nitric oxide (NO) levels. It also depleted antioxidant defences, including reduced glutathione (GSH) and superoxide dismutase (SOD). A robust inflammatory response was observed, with elevated levels of tumor necrosis factor -alpha (TNF-α), (NF-κB), and interleukin-6 (IL-6). The profibrotic cascade was activated through increased transforming growth factor beta 1(TGF-β1) and matrix metalloproteinase (MMP-2), alongside the upregulation of connective tissue growth factor (CTGF) and platelet derived growth factor (PDGF) mRNA. Apoptotic signalling was heightened by decreased B-cell lymphoma2 (Bcl-2) levels. Crucially, AMD downregulated SIRT1 and mitogen activated protein kinase (MAPK1/ERK2) mRNA expression. Conversely, NAR co-treatment significantly attenuated histopathological changes and reduced fibrosis scores. NAR effectively mitigated oxidative stress and restored antioxidant defenses. It also suppressed inflammatory and modulates anti-apoptotic signalling pathways. Notably, NAR decreased TGF-β1, MMP-2, CTGF, and PDGF, while restoring SIRT1 and MAPK1/ERK2 expression.
conclusionsNAR provides significant protection against AMD-induced PF by reducing oxidative stress, inflammation, and modulating anti-apoptotic signalling pathways. These effects are likely mediated through the modulation of the SIRT1/NF-κB signalling pathway. This suggests NAR as a potential therapeutic candidate for drug-induced lung injury.
Indexed as
Identifiers
42418051What OpenQuestion holds
Registered trials
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.