期刊
BIOENGINEERED
卷 13, 期 4, 页码 9233-9247出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/21655979.2022.2059995
关键词
Ellagic acid; osteoarthritis; oxidative stress; chondrocytes; nrf2
资金
- 'Science and Technology Innovation Action Program' Natural Science Foundation of Shanghai - Shanghai Science and Technology Commission [22ZR1410800, 21ZR1412100]
- National Natural Science Foundation of China [81672142]
- 'Shanghai `Rising Stars of Medical Talent' Youth Development Program Shanghai Municipal Health Commission [2019-72]
Osteoarthritis (OA) is a common degenerative joint disease associated with oxidative stress. Natural antioxidants, such as ellagic acid (EA), have potential in the management of OA. This study found that EA can attenuate IL-1beta-induced oxidative stress, protect chondrocytes from dysfunction, and upregulate the Keap1/Nrf2 signaling pathway.
Osteoarthritis (OA) is the most prevalent type of degenerative joint disease, and its pathological progression is highly associated with oxidative stress. Natural antioxidants can attenuate oxidative stress and chondrocyte injury, suggesting that antioxidants have potential applications in the management of OA. Ellagic acid (EA), a natural polyphenol derived from fruits or nuts, exerts antioxidant and anti-inflammatory effects in diseases related to oxidative stress. Herein, we investigated the effects of EA on interleukin-1 beta (IL-1 beta)-induced oxidative stress and degeneration in C28/I2 human chondrocytes. EA efficiently suppressed IL-1 beta-induced oxidative stress and ameliorated oxidative stress-induced dysfunction of chondrocytes, as indicated by the promotion of cartilage matrix secretion. Moreover, EA remarkably suppressed cell apoptosis and senescence, and reduced the expression of proinflammatory factors and metalloproteinases, suggesting that EA could alleviate chondrocyte injury under oxidative stress. Mechanistically, EA upregulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) as well as its downstream targets NADPH quinone oxidoreductase 1 and heme oxygenase-1. ML385, a specific Keap1/Nrf2 pathway inhibitor, blocked the antioxidant and chondroprotective effects of EA. Our findings demonstrated that EA could attenuate oxidative stress and exert protective effects on chondrocytes by upregulating the Keap1/Nrf2 signaling pathway.
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