Melatonin prevents pulmonary fibrosis caused by PM 2.5 exposure by targeting epithelial-mesenchymal transition.

Autor: Chen PC; School of Life Science, National Taiwan Normal University, Taipei, Taiwan; Translational medicine center, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei City, Taiwan; Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan., Yen MH; Department of Chest Surgery, Cathay General Hospital, New Taipei City, Taiwan., Hsiao SY; Division of Hematology-Oncology, Department of Internal Medicine, Chi Mei Medical Center, Liouying, Tainan, Taiwan; Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan., Kao WC; Division of Hematology-Oncology, Department of Internal Medicine, Chi Mei Medical Center, Liouying, Tainan, Taiwan., Wang MT; Division of Physical Medicine and Rehabilitation, Fu Jen Catholic University Hospital, Taipei, Taiwan, ROC., Chiou PC; Department of Respiratory Therapy, Fu Jen Catholic University, New Taipei City, Taiwan., Chao CC; Department of Respiratory Therapy, Fu Jen Catholic University, New Taipei City, Taiwan. Electronic address: 095457@mail.fju.edu.tw.
Jazyk: angličtina
Zdroj: Toxicology and applied pharmacology [Toxicol Appl Pharmacol] 2024 Jun; Vol. 487, pp. 116949. Date of Electronic Publication: 2024 Apr 28.
DOI: 10.1016/j.taap.2024.116949
Abstrakt: Pulmonary fibrosis is a lung disorder characterized by the accumulation of abnormal extracellular matrix, scar tissue formation, and tissue stiffness. Type II alveolar epithelial cells (AEII) play a critical role in repairing lung tissue after injury, and repeated injury to these cells is a key factor in the development of pulmonary fibrosis. Chronic exposure to PM 2.5 , a type of air pollution, has been shown to increase the incidence and severity of pulmonary fibrosis by enhancing the activation of EMT in lung epithelial cells. Melatonin, a hormone with antioxidant properties, has been shown to prevent EMT and reduce fibrosis in previous studies. However, the mechanism through which melatonin targets EMT to prevent pulmonary fibrosis caused by PM 2.5 exposure has not been extensively discussed before. In this current study, we found that melatonin effectively prevented pulmonary fibrosis caused by prolonged exposure to PM 2.5 by targeting EMT. The study demonstrated changes in cellular morphology and expression of EMT markers. Furthermore, the cell migratory potential induced by prolonged exposure to PM 2.5 was greatly reduced by melatonin treatment. Finally, in vivo animal studies showed reduced EMT markers and improved pulmonary function. These findings suggest that melatonin has potential clinical use for the prevention of pulmonary fibrosis.
Competing Interests: Declaration of competing interest The authors state no conflict of interest.
(Copyright © 2024 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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