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Validation of Active Compound of Terminalia catappa L. Extract and Its Anti-Inflammatory and Antioxidant Properties by Regulating Mitochondrial Dysfunction and Cellular Signaling Pathways

  • So Jeong Paik (School of Food Science and Biotechnology, Kyungpook National University) ;
  • Dong-Shin Kim (National Institute of Horticultural and Herbal Science, Rural Development Administration) ;
  • Joe Eun Son (School of Food Science and Biotechnology, Kyungpook National University) ;
  • Tran The Bach (Institute of Ecology and Biological Resources, Vietnam Academy of Science and Technology) ;
  • Do Van Hai (Institute of Ecology and Biological Resources, Vietnam Academy of Science and Technology) ;
  • Jin-Hyub Paik (International Biological Material Research Center, Korea Research Institute of Bioscience & Biotechnolog) ;
  • Sangjin Jo (International Biological Material Research Center, Korea Research Institute of Bioscience & Biotechnolog) ;
  • Dong Joon Kim (Department of Microbiology, College of Medicine, Dankook University) ;
  • Sung Keun Jung (School of Food Science and Biotechnology, Kyungpook National University)
  • Received : 2024.07.24
  • Accepted : 2024.08.27
  • Published : 2024.10.28

Abstract

As chronic inflammation and oxidative stress cause various diseases in the human body, this study aimed to develop functional materials to prevent inflammation and oxidative stress. This study investigated the biological function and components of Terminalia catappa L. extract prepared using its leaves and branches (TCE). TCE was determined using ultraperformance liquid chromatography-quadrupole-time-of-flight mass spectrometry. Using RAW 264.7 mouse macrophages, inhibitory effects of the identified compounds on nitric oxide (NO) and reactive oxygen species (ROS) generation were analyzed. Therefore, α-punicalagin was selected as an active compound with the highest content (986.6 ± 68.4 ㎍/g) and physiological activity. TCE exhibited an inhibitory effect on lipopolysaccharide (LPS)-induced inflammatory markers, including NO, inducible nitric oxide synthase, and inflammatory cytokines without exerting cytotoxicity. Moreover, TCE prevented excessive ROS production mediated by LPS and upregulated hemeoxygenase-1 expression via the nuclear translocation of nuclear factor erythroid 2-related factor 2. Interestingly, TCE prevented LPS-induced mitochondrial membrane potential loss, mitochondrial ROS production, and dynamin-related protein 1 phosphorylation (serine 616), a marker of abnormal mitochondrial fission. Furthermore, TCE considerably repressed the activation of LPS-induced mitogen-activated protein kinase pathway. Thus, TCE is a promising anti-inflammatory and antioxidant pharmaceutical or nutraceutical, as demonstrated via mitochondrial dysfunction and cellular signaling pathway regulation.

Keywords

Acknowledgement

This study was financially supported by the Basic Science Research Program through the National Research Foundation of Korea, which is funded by the Ministry of Education (NRF-2022R1A2C1010923); and the Korea Institute of Marine Science & Technology Promotion (KIMST) funded by the Ministry of Oceans and Fisheries (20220505). This study was also supported by the KRIBB Initiative Program of the Republic of Korea and project đTđL.CN-72/22 in Vietnam.

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