Sulforaphane attenuates pulmonary fibrosis by inhibiting the epithelial-mesenchymal transition
Kyung SY, Kim DY, Yoon JY, Son ES, Kim YJ, Park JW, Jeong SH
BMC pharmacology & toxicology · 93 citas
Etiquetas de revisión
Solo mecanismosDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
- Estudiado en
- Personas, más trabajo en animales o laboratorio
- Resultado principal
- Solo mecanismos
Quién lo pagó
- Financiación
- Financiación independiente
- Universidad u hospital
- Gachon University
- Universidad u hospital
- Gil Medical Center, Gachon University
- Universidad u hospital
- Gachon University Gil Medical Center
- Subvenciones
- Gil Medical Center, Gachon University (2013-34)
Según 3 financiadores declarados y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2018-04-02 · BMC Pharmacol Toxicol · vol. 19 · número 1 · pág. 13
- Editorial
- BioMed Central
- Citado
- 104 citas · más que el 97% de estudios similares · 5.7× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 35 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY
- Áreas de investigación
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis · Genomics, phytochemicals, and oxidative stress · IL-33, ST2, and ILC Pathways
- Palabras clave
- Epithelial–mesenchymal transition, Sulforaphane, Pulmonary fibrosis, Transition (genetics), Mesenchymal stem cell, Cancer research, Fibrosis, Cell biology, Chemistry, Medicine, Biology, Pathology, Biochemistry, Gene
- MeSH
- lung, cell line, animals, mice, inbred c57bl, humans, pulmonary fibrosis, isothiocyanates, sulfoxides, collagen type i, bleomycin, transforming growth factor beta, collagen type iv, male, smad2 protein, smad3 protein, epithelial-mesenchymal transition
7 autores
- Sun Young Kyung🇰🇷Gachon University; Gachon University Gil Medical Center
- Dae Young Kim🇰🇷Gachon University
- Jin Young Yoon🇰🇷Gachon University; Gachon University Gil Medical Center
- Eun Suk Son🇰🇷Gachon University; Gachon University Gil Medical Center
- Yu Jin Kim🇰🇷Gachon University; Gachon University Gil Medical Center
- Jeong Woong Park🇰🇷Gachon University; Gachon University Gil Medical Center
- Sung Hwan Jeong🇰🇷 · autor de correspondenciaGachon University; Gachon University Gil Medical Center
Resumen
El texto original del estudio, en el idioma en que se publicó.
Background
Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal disease with no effective treatment. The epithelial-mesenchymal transition (EMT) is a critical stage during the development of fibrosis. To assess the effect of sulforaphane (SFN) on the EMT and fibrosis using an in vitro transforming growth factor (TGF)-β1-induced model and an in vivo bleomycin (BLM)-induced model.
Methods
In vitro studies, cell viability, and cytotoxicity were measured using a Cell Counting Kit-8. The functional TGF-β1-induced EMT and fibrosis were assessed using western blotting and a quantitative real-time polymerase chain reaction. The lungs were analyzed histopathologically in vivo using hematoxylin and eosin and Masson's trichrome staining. The BLM-induced fibrosis was characterized by western blotting and immunohistochemical analyses for fibronectin, TGF-β1, E-cadherin (E-cad), and α-smooth muscle actin (SMA) in lung tissues.
Results
SFN reversed mesenchymal-like changes induced by TGF-β1 and restored cells to their epithelial-like morphology. The results confirmed that the expression of the epithelial marker, E-cadherin, increased after SFN treatment, while expression of the mesenchymal markers, N-cadherin, vimentin, and α-SMA decreased in A549 cells after SFN treatment. In addition, SFN inhibited TGF-β1-induced mRNA expression of the EMT-related transcription factors, Slug, Snail, and Twist. The SFN treatment attenuated TGF-β1-induced expression of fibrosis-related proteins, such as fibronection, collagen I, collagen IV, and α-SMA in MRC-5 cells. Furthermore, SFN reduced the TGF-β1-induced phosphorylation of SMAD2/3 protein in A549 cells and MRC-5 cells. BLM induced fibrosis in mouse lungs that was also attenuated by SFN treatment, and SFN treatment decreased BLM-induced fibronectin expression, TGF-β1 expression, and the levels of collagen I in the lungs of mice.
Conclusions
SFN showed a significant anti-fibrotic effect in TGF-β-treated cell lines and BLM-induced fibrosis in mice. These findings showed that SFN has anti-fibrotic activity that may be considered in the treatment of IPF.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).
Confianza de la comunidad
Cargando…
¿Cuánto confías en los hallazgos de este estudio?
Comentarios
¿Algo está mal aquí?
Señala este estudio si su información, etiquetas o financiación parecen incorrectas. Un editor revisa cada señalamiento.
Información educativa sobre investigación publicada. No es consejo médico ni una recomendación para empezar o dejar nada.