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Open AccessArticle

Cudratricusxanthone O Inhibits H2O2-Induced Cell Damage by Activating Nrf2/HO-1 Pathway in Human Chondrocytes

College of Pharmacy, Keimyung University, 1095 Dalgubeol-daero, Daegu 42601, Korea
*
Author to whom correspondence should be addressed.
These two authors contributed equally to this work.
Antioxidants 2020, 9(9), 788; https://doi.org/10.3390/antiox9090788
Received: 24 July 2020 / Revised: 21 August 2020 / Accepted: 23 August 2020 / Published: 25 August 2020
(This article belongs to the Special Issue Oxidative Stress Modulators and Functional Foods)
Osteoarthritis (OA) is a common joint degenerative disease induced by oxidative stress in chondrocytes. Although induced-heme oxygenase-1 (HO-1) has been found to protect cells against oxygen radical damage, little information is available regarding the use of bioactive compounds from natural sources for regulating the HO-1 pathway to treat OA. In this study, we explored the inhibitory effects of cudratricusxanthone O (CTO) isolated from the Maclura tricuspidata Bureau (Moraceae) on H2O2-induced damage of SW1353 chondrocytes via regulation of the HO-1 pathway. CTO promoted HO-1 expression by enhancing the translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) into the nucleus without inducing toxicity. Pretreatment with CTO-regulated reactive oxygen species (ROS) production by inducing expression of antioxidant enzymes in H2O2-treated cells and maintained the functions of H2O2-damaged chondrocytes. Furthermore, CTO prevented H2O2-induced apoptosis by regulating the expression of anti-apoptotic proteins. Treatment with the HO-1 inhibitor tin-protoporphyrin IX revealed that these protective effects were exerted due to an increase in HO-1 expression induced by CTO. In conclusion, CTO protects chondrocytes from H2O2-induced damages—including ROS accumulation, dysfunction, and apoptosis through activation of the Nrf2/HO-1 signaling pathway in chondrocytes and, therefore, is a potential therapeutic agent for OA treatment. View Full-Text
Keywords: cudratrixanthone O; reactive oxygen species; nuclear transcription factor erythroid-2-like factor 2; hemeoxygenase-1; apoptosis cudratrixanthone O; reactive oxygen species; nuclear transcription factor erythroid-2-like factor 2; hemeoxygenase-1; apoptosis
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MDPI and ACS Style

Kim, E.-N.; Lee, H.-S.; Jeong, G.-S. Cudratricusxanthone O Inhibits H2O2-Induced Cell Damage by Activating Nrf2/HO-1 Pathway in Human Chondrocytes. Antioxidants 2020, 9, 788. https://doi.org/10.3390/antiox9090788

AMA Style

Kim E-N, Lee H-S, Jeong G-S. Cudratricusxanthone O Inhibits H2O2-Induced Cell Damage by Activating Nrf2/HO-1 Pathway in Human Chondrocytes. Antioxidants. 2020; 9(9):788. https://doi.org/10.3390/antiox9090788

Chicago/Turabian Style

Kim, Eun-Nam; Lee, Hyun-Su; Jeong, Gil-Saeng. 2020. "Cudratricusxanthone O Inhibits H2O2-Induced Cell Damage by Activating Nrf2/HO-1 Pathway in Human Chondrocytes" Antioxidants 9, no. 9: 788. https://doi.org/10.3390/antiox9090788

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