Journal Article Ppublish
PubMed: 40226757 DOI: 10.4162/nrp.2025.19.2.170
Linn flower extract inhibits particulate matter 2.5-promoted epithelial-mesenchymal transition by attenuating reactive oxygen species generation in human retinal pigment epithelial ARPE-19 cells.
Nutr Res Pract 19(2):170-185
Authors: Beom Su Park, EunJin Bang, Hyesook Lee, Gi-Young Kim, Yung Hyun Choi
Affiliations
- Basic Research Laboratory for the Regulation of Microplastic-Mediated Diseases and Anti-Aging Research Center, Dong-eui University, Busan 47227, Korea. Department of Biochemistry, College of Korean Medicine, Dong-eui University, Busan 47227, Korea.
- Department of Convergence Medicine, Pusan National University School of Medicine, Yangsan 50612, Korea.
- Laboratory of Immunobiology, Department of Marine Life Sciences, Jeju National University, Jeju 63243, Korea.
Abstract
BACKGROUND/OBJECTIVES
Particulate matter 2.5 (PM2.5) exposure can promote epithelial-mesenchymal transition (EMT) in human retinal pigment epithelial (RPE) cells. The flowers of Linn, commonly known as marigold, are rich in diverse flavonoids and carotenoids and play a significant role in preventing cellular damage induced by oxidative stress, but the role of their extracts in RPE cells has not been reported. This study aimed to evaluate the influence of an ethanol extract of Linn flower (TE) on PM2.5-induced EMT processes in RPE ARPE-19 cells.
MATERIALS/METHODS
To investigate the protective effect of TE against ARPE-19 cell damage following PM2.5 treatment, cells were exposed to TE for 1 h before exposure to PM2.5 for 24 h. We investigated whether the efficacy of TE on suppressing PM2.5-induced EMT was related to antioxidant activity and the effect on the expression changes of factors involved in EMT regulation. Additionally, we further explored the role of intracellular signaling pathways associated with EMT inhibition.
RESULTS
TE significantly blocked PM2.5-induced cytotoxicity while effectively preventing mitochondrial dysfunction, increased reactive oxygen species (ROS) generation, and mitochondrial membrane potential disruption. TE inhibited PM2.5-induced EMT and inflammatory response by suppressing the ROS-mediated transforming growth factor-β/suppressor of mothers against decapentaplegic/mitogen-activated protein kinases signaling pathway.
CONCLUSION
Our results suggest that marigold extract is a highly effective in protection against PM2.5-induced eye damage.
MeSH
Cells, Transforming Growth Factors, Epithelial-Mesenchymal Transition, Retinal Pigments, Retinaldehyde, Particulate Matter