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C-Peptide Ameliorates Particulate Matter 2.5-Induced Skin Cell Apoptosis by Inhibiting NADPH Oxidation

  • Pincha Devage Sameera Madushan Fernando (Department of Biochemistry, College of Medicine, and Jeju Research Center for Natural Medicine, Jeju National University) ;
  • Mei Jing Piao (Department of Biochemistry, College of Medicine, and Jeju Research Center for Natural Medicine, Jeju National University) ;
  • Herath Mudiyanselage Udari Lakmini Herath (Department of Biochemistry, College of Medicine, and Jeju Research Center for Natural Medicine, Jeju National University) ;
  • Kyoung Ah Kang (Department of Biochemistry, College of Medicine, and Jeju Research Center for Natural Medicine, Jeju National University) ;
  • Kwon-Soo Ha (Department of Molecular and Cellular Biochemistry, Kangwon National University School of Medicine) ;
  • Sungwook Chae (KM Convergence Research Division, Korea Institute of Oriental Medicine) ;
  • Jin Won Hyun (Department of Biochemistry, College of Medicine, and Jeju Research Center for Natural Medicine, Jeju National University)
  • Received : 2024.04.02
  • Accepted : 2024.09.30
  • Published : 2025.01.01

Abstract

Connecting peptide (C-peptide), a byproduct of insulin biosynthesis, has diverse cellular and biological functions. Particulate matter 2.5 (PM2.5) adversely affects human skin, leading to skin thickening, wrinkle formation, skin aging, and inflammation. This study aimed to investigate the protective effects of C-peptide against PM2.5-induced damage to skin cells, focusing on oxidative stress as a key mechanism. C-peptide mitigated NADPH oxidation and intracellular reactive oxygen species (ROS) production induced by PM2.5. It also suppressed PM2.5-induced NADPH oxidase (NOX) activity and alleviated PM2.5-induced NOX1 and NOX4 expression. C-peptide protected against PM2.5-induced DNA damage, lipid peroxidation, and protein carbonylation. Additionally, C-peptide mitigated PM2.5-induced apoptosis by inhibiting intracellular ROS production. In summary, our findings suggest that C-peptide mitigates PM2.5-induced apoptosis in human HaCaT keratinocytes by inhibiting intracellular ROS production and NOX activity.

Keywords

Acknowledgement

This study was supported by the Basic Research Laboratory Program (NRF-2017R1A4A1014512) from the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT, and Future Planning. This research was also supported by the Basic Science Research Program through NRF, funded by the Ministry of Education (RS-2023-00270936).

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