Suppressive Activities of Fisetin on Particulate Matter-induced Oxidative Stress

• Published in: Biotechnology and bioprocess engineering Vol. 26; no. 4; pp. 568 - 574
• Main Authors: Sim, Hyunchae, Noh, Yeeun, Choo, Samyeol, Kim, Nayeon, Lee, Taeho, Bae, Jong-Sup
• Format: Journal Article
• Language: English
• Published: Seoul The Korean Society for Biotechnology and Bioengineering 01.08.2021; Springer Nature B.V; 한국생물공학회
• Subjects: aerodynamics; Antioxidants; Antiviral drugs; bioprocessing; Biotechnology; Catalase; Cell survival; Cell viability; Chemistry; Chemistry and Materials Science; Damage; dose response; Endothelial cells; Glucocorticoids; humans; Industrial and Production Engineering; Inflammation; Intracellular; Kinases; L-Lactate dehydrogenase; Lactate dehydrogenase; Lactic acid; Neuroprotection; Oxidative stress; Particulate emissions; Particulate matter; particulates; protective effect; Pulmonary arteries; Pulmonary artery; Reactive oxygen species; Research Paper; Superoxide dismutase; Survival factor; Toxicity; viability assays; 생물공학; fisetin; oxidation; particulate matter; ROS
• ISSN: 1226-8372; 1976-3816
• DOI: 10.1007/s12257-021-0050-0

Exposure to high levels of atmospheric particulate matter (PM) with an aerodynamic diameter of less than 2.5 µm (PM 2.5 ) 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 PM 2.5 -induced toxicity in human pulmonary artery endothelial cells (HPAECs) and its molecular mechanism. Exposure to PM 2.5 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 PM 2.5 -induced oxidative stress in a dose-dependent manner. Serum- and glucocorticoid-inducible kinase 1 (SGK1), a crucial cell survival factor, was downregulated by PM 2.5 which was recovered by fisetin. Furthermore, fisetin treatment inhibited intracellular ROS in HPAECs generated by PM 2.5 . Moreover, decreased antioxidant enzymes activities of superoxide dismutase and catalase level in PM 2.5 -treated cells were reversed by fisetin treatment. Our results suggest that fisetin effectively protects human HPAECs from PM 2.5 -induced oxidative damage via antioxidant effects.