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Inhibition of keloid by (32)P isotope radiotherapy through suppressing TGF-β/Smad signaling pathway

Background: Keloid seriously affects the appearance, and is accompanied by some symptoms including pain, burning, itching. Radioactive nuclides such as (32)P have been proved to be effective in inhibiting the formation of keloid, but the mechanism remains unclear. Methods: The keloid animal model wa...

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Detalles Bibliográficos
Autores principales: Xie, Long, Huang, Liqun, Zhang, Guanjie, Su, Yingrui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10683590/
https://www.ncbi.nlm.nih.gov/pubmed/37910782
http://dx.doi.org/10.18632/aging.205160
Descripción
Sumario:Background: Keloid seriously affects the appearance, and is accompanied by some symptoms including pain, burning, itching. Radioactive nuclides such as (32)P have been proved to be effective in inhibiting the formation of keloid, but the mechanism remains unclear. Methods: The keloid animal model was established through keloid tissues implantation. Hematoxylin-Eosin (HE) and Masson staining were performed to investigate histological changes and collagen deposition. The mRNA and protein expression were assessed using RT-PCR and western blotting, respectively. Cell apoptosis and cycle were evaluated through flow cytometry. Results: Both (32)P isotope injection and skin path significantly reduced the size of keloid, and inhibited TGF-β/Smad signaling pathway. SRI-011381, the agonist of TGF-β/Smad signaling pathway, markedly reversed the influence of (32)P isotope on cell proliferation, cell apoptosis, cell cycle of LNCaP cells and TGF-β/Smad signaling pathway. Conclusions: (32)P isotope injection and skin path greatly reduced the size of keloid, and the TGF-β/Smad signaling pathway was remarkably inhibited by (32)P isotope treatment. The regulation of dermal fibroblast by (32)P isotope was reversed by SRI-011381. (32)P isotope might inhibit keloid through suppressing TGF-β/Smad signaling pathway. Our study provides a novel therapeutic strategy for the treatment of keloid.