ArticlePloS one2025
Effect and mechanism of Nintedanib on acute and chronic radiation-induced lung injury in mice.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Integrated machine learning risk model for predicting radiation pneumonitis in lung cancer patients with interstitial lung disease.Annals of medicine · 2026Article
- Unraveling the molecular landscape of chronic radiation injury: From oxidative stress signaling to translational modeling (Review).International journal of molecular medicine · 2026Review
- Interpreting the Black Box: Interpretable Machine Learning and Systems Pharmacology in Small-Molecule Therapeutics.Pharmaceutics · 2026Review
- Nintedanib Lacks Efficacy in a Spirometry-Confirmed and Bleomycin-Induced Mouse Model of Idiopathic Pulmonary Fibrosis.Basic & clinical pharmacology & toxicology · 2026Article
- Radiomitigators: Breakthroughs in Post-Radiation Recovery.Antioxidants (Basel, Switzerland) · 2026Review
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Authors and funding
3 authors.
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Abstract
objectiveTo investigate the efficacy of Nintedanib in treating acute and chronic radiation-induced lung injury and its mechanism of action.
methodsA radiation-induced lung injury model was established in mice using 6MV X-rays at 18Gy to irradiate the lungs. The mice were randomly divided into four groups: control group, radiation therapy group, low-dosage Nintedanib + radiation therapy group, and high dosage Nintedanib + radiation therapy group. The mice were euthanized on day 14 and 3 months post-radiation to observe changes in acute and chronic inflammation and the expression of related proteins.
resultsCompared to the radiation therapy group, the low and high-dosage Nintedanib groups showed varying degrees of improvement in mental state, responsiveness, food and water intake, and fur condition. During the acute inflammatory phase, HE staining revealed inflammatory changes in the lung tissues of both Nintedanib groups, but the pathology was less severe than in the radiation group, with the high-dosage group showing more significant reduction. Serum levels of IL-6, TNF-α and TGF-β1 were significantly reduced (P < 0.05), suggesting that Nintedanib can decrease the expression of serum inflammatory factors. The percentage of Smad2-positive area in the low and high-dosage Nintedanib groups was (7.395 ± 0.90)% and (5.577 ± 1.56)%, respectively, both significantly lower than the radiation group (P < 0.05). At 3 months post-radiation, Masson's trichrome staining showed that the Ashcroft score in the Nintedanib groups was significantly lower than in the radiation group (P < 0.05). There were statistically significant differences between the low and high-dosage groups in the percentage of Smad2 and αSMA-positive areas and the levels of serum TGF-β1 (all P < 0.05), and both were significantly lower compared to the radiation group (P < 0.05).
conclusion(1) Nintedanib can improve the general condition of mice with acute and chronic radiation-induced lung injury and reduce pathological damage to lung tissue. (2) Nintedanib may exert a protective effect on mice with acute and chronic radiation-induced lung injury by downregulating the TGF-β1/Smad2 signaling pathway, thereby inhibiting inflammatory and fibrotic responses.
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