Biotechnology and Bioprocess Engineering 2021; 26(4): 568-574  
Suppressive Activities of Fisetin on Particulate Matter-induced Oxidative Stress
Hyunchae Sim, Yeeun Noh, Samyeol Choo, Nayeon Kim, Taeho Lee, and Jong-Sup Bae
Hyunchae Sim, Yeeun Noh, Samyeol Choo, Nayeon Kim, Taeho Lee*, Jong-Sup Bae*
College of Pharmacy, Research Institute of Pharmaceutical Sciences, Kyungpook National University, Daegu 41566, Korea
Tel: +82-53-950-8573; Fax: +82-53-950-8557
E-mail: tlee@knu.ac.kr
Tel: +82-53-950-8570; Fax: +82-53-950-8557
E-mail: baejs@knu.ac.kr
These authors contributed equally.
Received: February 24, 2021; Revised: March 8, 2021; Accepted: March 8, 2021; Published online: August 30, 2021.
© The Korean Society for Biotechnology and Bioengineering. All rights reserved.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Exposure to high levels of atmospheric particulate matter (PM) with an aerodynamic diameter of less than 2.5 μm (PM2.5) causes respiratory injury mainly due to oxidative stress. Although the fisetin has biological activities such as the antiviral, neuroprotective, and anti-inflammatory activities, the effect of fisetin on PM-mediated oxidative damage has not been studied. In this study, we tested the protective effect of fisetin against PM2.5-induced toxicity in human pulmonary artery endothelial cells (HPAECs) and its molecular mechanism. Exposure to PM2.5 decreased cell viability in HPAECs in a time- and dose-dependent manner, possibly due to increased release of extracellular lactate dehydrogenase and generation of intracellular reactive oxygen species (ROS). Cell viability assay demonstrated that treatment of HPAECs with fisetin increased cell viability and reduced PM2.5-induced oxidative stress in a dose-dependent manner. Serum- and glucocorticoid-inducible kinase 1 (SGK1), a crucial cell survival factor, was downregulated by PM2.5 which was recovered by fisetin. Furthermore, fisetin treatment inhibited intracellular ROS in HPAECs generated by PM2.5. Moreover, decreased antioxidant enzymes activities of superoxide dismutase and catalase level in PM2.5-treated cells were reversed by fisetin treatment. Our results suggest that fisetin effectively protects human HPAECs from PM2.5-induced oxidative damage via antioxidant effects.
Keywords: fisetin, particulate matter, oxidation, ROS


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