Avaliação do cinamato de metila sobre as funções das células epiteliais estimuladas por TGF-β1

Abstract

Pulmonary fibrosis is a chronic, fibroproliferative pathology characterised by the exacerbated deposition of extracellular matrix (ECM), in which epithelial cells undergoing the process of epithelial-mesenchymal transdifferentiation (EMT) play a relevant role in the fibrogenic process. During EMT, epithelial cells lose their original phenotypic characteristics and acquire mesenchymal properties, such as greater motility and excessive production of ECM. Previous studies indicate that methyl cinnamate (MC) has antioxidant and anti-inflammatory properties; however, its antifibrotic effects have not yet been investigated. In this study, we evaluated the effects of CM on human alveolar epithelial cells induced to undergo EMT after stimulation with TGF-β1. Human epithelial A549 cells were exposed to CM and had their cell viability assessed using the MTT assay. Our results showed that CM was not cytotoxic at the concentrations analysed. EMT was confirmed after 24 hours of stimulation with TGF-β1, evidenced by distinct morphological changes and increased expression of mesenchymal markers such as vimentin. However, treatment with CM resulted in a significant reduction in the expression of this marker. Additionally, the cell migration assay revealed that CM inhibited the increase in the migration rate of mesenchymal cells induced by TGF-β1. These findings indicate that methyl cinnamate may be useful as a modulating agent for the cellular processes associated with fibrosis, indicating its possible application in controlling the progression of this pathology.