Cytoprotective Effects of Delphinidin for Human Chondrocytes against Oxidative Stress through Activation of Autophagy
1
Department of Orthopaedic Surgery, Armed Forces Daegu Hospital, Gyeongsan 38427, Korea
2
Department of Medicine, Gyeongsang National University School of Medicine, Jinju 52727, Korea
3
Department of Orthopaedic Surgery, Institute of Health Science, Gyeongsang National University Hospital and Gyeongsang National University School of Medicine, Jinju 52727, Korea
4
Department of Biochemistry and Convergence Medical Science, Institute of Health Science, Gyeongsang National University School of Medicine, Jinju 52727, Korea
*
Authors to whom correspondence should be addressed.
†
These authors contribute equally to this work.
Antioxidants 2020, 9(1), 83; https://doi.org/10.3390/antiox9010083
Received: 19 December 2019
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Revised: 15 January 2020
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Accepted: 16 January 2020
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Published: 19 January 2020
(This article belongs to the Special Issue Antioxidant and Cytoprotective Activity)
Antioxidant enzymes are decreased in osteoarthritis (OA) patients, implying the role of oxidative stress in osteoarthritis pathogenesis. The aim of this study was to evaluate the cytoprotective effects of delphinidin, a potent antioxidant, in human chondrocytes and the underlying mechanisms. The cytoprotective mechanism induced by delphinidin against oxidative stress (H2O2) in human chondrocytes was investigated. Cell viability and death were evaluated using proapoptotic and antiapoptotic markers such as cleaved caspase-3 (c-caspase-3), cleaved poly(ADP-ribose) polymerase N-acetylcysteine (c-PARP), Bcl-XL, and transcription factors associated with redox and inflammation regulation, including nuclear factor kappa B (NF-κB) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Induction of autophagy was assessed by formation of LC3-II and autophagosome-(LC3 punctate, monodansylcadaverine (MDC) and acridine orange staining) in the presence or absence of an autophagy inhibitor. Treatment with delphinidin itself at concentration below 50 µM for 24 h did not affect viability of chondrocytes. Delphinidin inhibited reactive oxygen species (ROS)-induced apoptosis by significantly decreasing apoptosis markers such as c-caspase-3 and c-PARP while increasing antiapoptotic marker Bcl-XL and antioxidant response NF-κB and Nrf2 pathways. Delphinidin also activated cytoprotective autophagy to protect chondrocytes during oxidative stresses. Activation of autophagy with autophagy inducer rapamycin also inhibited ROS-induced cell death and decreased proapoptotic proteins but increased antiapoptotic protein Bcl-XL, NF-κB, and Nrf2. Delphinidin can protect chondrocytes against H2O2-induced apoptosis via activation of Nrf2 and NF-κB and protective autophagy. Thus, it can inhibit OA with protection of chondrocytes. Delphinidin can protect chondrocytes against H2O2-induced ROS with maintenance of homeostasis and redox. These results suggest that delphinidin could be used to protect chondrocytes against age-related oxidative stress and other oxidative stresses in the treatment of OA. Thus, delphinidin may play a critical role in preventing the development and progression of OA.
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Keywords:
osteoarthritis; oxidative stress; apoptosis; autophagy; delphinidin; Nrf2
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MDPI and ACS Style
Lee, D.-Y.; Park, Y.-J.; Song, M.-G.; Kim, D.R.; Zada, S.; Kim, D.-H. Cytoprotective Effects of Delphinidin for Human Chondrocytes against Oxidative Stress through Activation of Autophagy. Antioxidants 2020, 9, 83. https://doi.org/10.3390/antiox9010083
AMA Style
Lee D-Y, Park Y-J, Song M-G, Kim DR, Zada S, Kim D-H. Cytoprotective Effects of Delphinidin for Human Chondrocytes against Oxidative Stress through Activation of Autophagy. Antioxidants. 2020; 9(1):83. https://doi.org/10.3390/antiox9010083
Chicago/Turabian StyleLee, Dong-Yeong, Young-Jin Park, Myung-Geun Song, Deok R. Kim, Sahib Zada, and Dong-Hee Kim. 2020. "Cytoprotective Effects of Delphinidin for Human Chondrocytes against Oxidative Stress through Activation of Autophagy" Antioxidants 9, no. 1: 83. https://doi.org/10.3390/antiox9010083
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