ArticleApplied biochemistry and biotechnology2026
Dietary Chlorogenic Acid and Omega-3 Relieve Methotrexate-Induced Lung Injury Through Modulation of SIRT1/ PGC-1α/ NF-κB Signaling Axis.
Article in Applied biochemistry and biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methotrexate (MTX) is a pivotal chemotherapeutic drug which is also used to treat serious chronic inflammatory disorders. However, it causes perilous pulmonary injury. This study aimed to explore the protective effects of CGA and ω-3 on MTX-induced pulmonary toxicity in rats via modulation of SIRT1/PGC-1α/ NF-κB signaling axis. Twenty-four male Sprague-Dawley rats were randomly divided into four groups; normal, MTX, MTX + CGA, and MTX + ω-3, rats were injected with MTX single dose intraperitoneally (20 mg/kg) followed by an oral administration of CGA (100 mg/kg) or ω-3 (400 mg/kg) for seven days. Both CGA and ω-3 relieved MTX-induced-pulmonary histopathological changes by decreasing alveolar epithelial loss and inflammatory cell infiltration. Also, CGA and ω-3 markedly ameliorated the oxidative stress by lowering pulmonary MDA content along with significant increment in pulmonary GSH content. Moreover, both CGA and ω-3 suppressed pulmonary inflammation as proved by marked lowering of serum CRP level via downregulation of pulmonary NF-κB, TNF-α and MPO levels along with upregulation of pulmonary SIRT1/PGC-1α expression and IL-10 level. Additionally, the antioxidant and anti-inflammatory activities of CGA and ω-3 promote pulmonary Bcl-2 expression and inhibit pulmonary caspase 3 expression which in turn suppress apoptotic cell death in the lungs of MTX-intoxicated rats. These protective effects of CGA and ω-3 suggest the potentiality of using them in conjunction with MTX treatment protocols to diminish their undesirable lung toxicity.
Indexed as
Identifiers
42108368What 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.