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dc.contributor.authorThanyaluck Phitaken_US
dc.contributor.authorPeraphan Pothacharoenen_US
dc.contributor.authorJongkolnee Settakornen_US
dc.contributor.authorWilart Poompimolen_US
dc.contributor.authorBruce Catersonen_US
dc.contributor.authorPrachya Kongtawelerten_US
dc.date.accessioned2018-09-04T05:59:37Z-
dc.date.available2018-09-04T05:59:37Z-
dc.date.issued2012-08-01en_US
dc.identifier.issn00319422en_US
dc.identifier.other2-s2.0-84863628193en_US
dc.identifier.other10.1016/j.phytochem.2012.05.016en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84863628193&origin=inwarden_US
dc.identifier.urihttp://cmuir.cmu.ac.th/jspui/handle/6653943832/51265-
dc.description.abstractOsteoarthritis (OA) is a major disability of elderly people. Sesamin is the main compound in Sesamun indicum Linn., and it has an anti-inflammatory effect by specifically inhibiting Δ5-desaturase in polyunsaturated fatty acid biosynthesis. The chondroprotective effects of sesamin were thus studied in a porcine cartilage explant induced with interleukin-1beta (IL-1β) and in a papain-induced osteoarthritis rat model. With the porcine cartilage explant, IL-1β induced release of sulfated-glycosaminoglycan (s-GAG) and hydroxyproline release, and this induction was significantly inhibited by sesamin. This ability to inhibit these processes might be due to its ability to decrease expression of MMP-1, -3 and -13, which can degrade both PGs and type II collagen, both at the mRNA and protein levels. Interestingly, activation of MMP-3 might also be inhibited by sesamin. Moreover, in human articular chondrocytes (HACs), some pathways of IL-1β signal transduction were inhibited by sesamin: p38 and JNK. In the papain-induced OA rat model, sesamin treatment reversed the following pathological changes in OA cartilage: reduced disorganization of chondrocytes in cartilage, increased cartilage thickness, and decreased type II collagen and PGs loss. Sesamin alone might increase formation of type II collagen and PGs in the cartilage tissue of control rats. These results demonstrate that sesamin efficiently suppressed the pathological processes in an OA model. Thus, sesamin could be a potential therapeutic strategy for treatment of OA. © 2012 Elsevier Ltd. All rights reserved.en_US
dc.subjectAgricultural and Biological Sciencesen_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleChondroprotective and anti-inflammatory effects of sesaminen_US
dc.typeJournalen_US
article.title.sourcetitlePhytochemistryen_US
article.volume80en_US
article.stream.affiliationsChiang Mai Universityen_US
article.stream.affiliationsRajabhat Universityen_US
article.stream.affiliationsCardiff Universityen_US
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