Please use this identifier to cite or link to this item: https://doi.org/10.3390/antiox10060862
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dc.titleCardamonin attenuates inflammation and oxidative stress in interleukin-1?-stimulated osteoarthritis chondrocyte through the nrf2 pathway
dc.contributor.authorPeng, Yi-Jen
dc.contributor.authorLu, Jeng-Wei
dc.contributor.authorLee, Chian-Her
dc.contributor.authorLee, Herng-Sheng
dc.contributor.authorChu, You-Hsiang
dc.contributor.authorHo, Yi-Jung
dc.contributor.authorLiu, Feng-Cheng
dc.contributor.authorHuang, Chun-Jung
dc.contributor.authorWu, Chia-Chun
dc.contributor.authorWang, Chih-Chien
dc.date.accessioned2022-10-12T08:05:53Z
dc.date.available2022-10-12T08:05:53Z
dc.date.issued2021-05-27
dc.identifier.citationPeng, Yi-Jen, Lu, Jeng-Wei, Lee, Chian-Her, Lee, Herng-Sheng, Chu, You-Hsiang, Ho, Yi-Jung, Liu, Feng-Cheng, Huang, Chun-Jung, Wu, Chia-Chun, Wang, Chih-Chien (2021-05-27). Cardamonin attenuates inflammation and oxidative stress in interleukin-1?-stimulated osteoarthritis chondrocyte through the nrf2 pathway. Antioxidants 10 (6) : 862. ScholarBank@NUS Repository. https://doi.org/10.3390/antiox10060862
dc.identifier.issn2076-3921
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/232458
dc.description.abstractOsteoarthritis (OA) is a chronic degenerative joint disease characterized by the deterioration of articular cartilage. The progression of OA leads to an increase in inflammatory mediators in the joints, thereby promoting the destruction of the cartilage matrix. Recent studies have reported on the anti-inflammatory and antioxidant properties of cardamonin, which also appears to interact with cellular targets, such as nuclear erythroid 2-related factor 2 (Nrf2), extracellular signal-regulated kinase (ERK), and mammalian target of rapamycin (mTOR) during the progression of tumors. To date, few studies have investigated the effects of cardamonin on chondrocyte inflammation. In the current study, we determined that treating interleukin-1 beta (IL-1?-stimulated chondrocyte cells) with cardamonin significantly reduced the release of nitric oxide (NO) and prostaglandin E2 (PGE2) and significantly inhibited the expression of pro-inflammatory proteins, including inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX2). Cardamonin was also shown to: (1) inhibit the activation and production of matrix metalloproteinases (MMPs), (2) suppress the nuclear factor-?B (NF-?B) signaling pathway, (3) suppress the expression of toll-like receptor proteins, (4) activate the Nrf2 signaling pathway, and (5) increase the levels of antioxidant proteins heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1). The increase in antioxidant proteins led to corresponding antioxidant effects (which were abolished by Nrf2 siRNA). Our findings identify cardamonin as a candidate Nrf2 activator for the treatment and prevention of OA related to inflammation and oxidative stress. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.
dc.publisherMDPI
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.sourceScopus OA2021
dc.subjectCardamonin
dc.subjectChondrocyte
dc.subjectInterleukin-1 beta
dc.subjectOsteoarthritis
dc.subjectOxidative stress
dc.typeArticle
dc.contributor.departmentDEPT OF BIOLOGICAL SCIENCES
dc.description.doi10.3390/antiox10060862
dc.description.sourcetitleAntioxidants
dc.description.volume10
dc.description.issue6
dc.description.page862
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