Please use this identifier to cite or link to this item: https://doi.org/10.3390/nu11051180
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dc.titleChondroprotective effects of genistein against osteoarthritis induced joint inflammation
dc.contributor.authorLiu, F.-C.
dc.contributor.authorWang, C.-C.
dc.contributor.authorLu, J.-W.
dc.contributor.authorLee, C.-H.
dc.contributor.authorChen, S.-C.
dc.contributor.authorHo, Y.-J.
dc.contributor.authorPeng, Y.-J.
dc.date.accessioned2021-12-29T04:35:51Z
dc.date.available2021-12-29T04:35:51Z
dc.date.issued2019
dc.identifier.citationLiu, F.-C., Wang, C.-C., Lu, J.-W., Lee, C.-H., Chen, S.-C., Ho, Y.-J., Peng, Y.-J. (2019). Chondroprotective effects of genistein against osteoarthritis induced joint inflammation. Nutrients 11 (5) : 1180. ScholarBank@NUS Repository. https://doi.org/10.3390/nu11051180
dc.identifier.issn20726643
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/212309
dc.description.abstractGenistein is an isoflavone extracted from soybean (Glycine max). This compound has anti-inflammatory, anti-oxidative, and anti-cancer effects; however, the mechanism underlying the effects of genistein on IL-1?-stimulated human osteoarthritis (OA) chondrocytes remains unknown. Our objectives in this study were to explore the anti-inflammatory effects of genistein on IL-1?-stimulated human OA chondrocytes and to investigate the potential mechanisms which underlie them. Our results from an in-vitro model of osteoarthritis indicate that genistein inhibits the IL-1?-induced expression of the catabolic factors nitric oxide synthase 2 (NOS2), cyclooxygenase 2 (COX-2), and matrix metalloproteinases (MMPs). Genistein was shown to stimulate Ho-1 expression, which has been associated with Nrf-2 pathway activation in human chondrocytes. In a rat model, genistein was also shown to attenuate the progression of traumatic osteoarthritis. Taken together, these results demonstrate the effectiveness of genistein in mediating the inflammation associated with joint disorders. Our results also indicate that genistein could potentially serve as an alternative therapeutic treatment for OA. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
dc.publisherMDPI AG
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.sourceScopus OA2019
dc.subjectGenistein
dc.subjectIL-1?
dc.subjectInflammation
dc.subjectOsteoarthritis
dc.typeArticle
dc.contributor.departmentBIOLOGICAL SCIENCES
dc.description.doi10.3390/nu11051180
dc.description.sourcetitleNutrients
dc.description.volume11
dc.description.issue5
dc.description.page1180
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