ArticleDose-response : a publication of International Hormesis Society
Radiation Protection of Polydatin Against Radon Exposure Injury of Epithelial Cells and Mice.
Article in Dose-response : a publication of International Hormesis Society. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- The pentose phosphate pathway contributes to excess lactate production in radiation-induced fibroblast to myofibroblast transdifferentiation.The Journal of biological chemistry · 2026Article
- Polydatin in respiratory diseases: multi-target mechanisms and therapeutic potential.Frontiers in pharmacology · 2026Review
- Prevention and treatment of radiation injury by traditional Chinese medicine: A review.Chinese herbal medicines · 2025Review
- Polydatin ameliorates hyperhidrosis by targeting Aqp5 in a mouse model.Frontiers in pharmacology · 2025Article
- Lactate exacerbates lung damage induced by nanomicroplastic through the gut microbiota-HIF1a/PTBP1 pathway.Experimental & molecular medicine · 2023Article
- Advancing Dose-Response Research: Integrating Exposome, Multi-Omics, and Low-Dose Phenomena in Toxicology and Medicine.Dose-response : a publication of International Hormesis SocietyArticle
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radon exposure is significantly associated with lung cancer. Radon concentration is currently reduced mainly by physical methods, but there is a lack of protective drugs or biochemical reagents for radon damage. This study aimed to explore the protective effect of polydatin (PD) on the radon-exposed injury. The results showed that PD can significantly reduce ROS level, raise SOD activity, weaken the migration ability, increase E-cad, and decrease mesenchymal cell surface markers (FN1, Vimentin, N-cad, α-SMA, and Snail) in radon-exposed epithelial cells. In vivo, PD increased the mice weight, promoted SOD activity, and decreased MDA content, the number of bullae, pulmonary septum thickness, lung collagenous fibers, and mesenchymal cell surface markers. Furthermore, PD inhibited p-PI3K, p-AKT, and p-mTOR expression. Compared with directly adding PD on radon-exposed cells, adding PD before and after radon exposure could more obviously improve the adhesion of radon-exposed cells, significantly alleviate the migration ability, and more significantly reduce mesenchyme markers and p-AKT and p-mTOR. These results indicate that PD can reduce oxidative stress, weaken epithelial-mesenchymal transition (EMT) and lung fibrosis in radon-exposed cells/mice, and have good radiation protection against radon injury. The mechanism is related to the inhibition of the PI3K/AKT/mTOR pathway.
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