Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/54157
Title: Suppression of inflammatory responses by black rice extract in RAW 264.7 macrophage cells via downregulation of NF-kB and AP-1 signaling pathways
Authors: Pornngarm Limtrakul
Supachai Yodkeeree
Pornsiri Pitchakarn
Wanisa Punfa
Authors: Pornngarm Limtrakul
Supachai Yodkeeree
Pornsiri Pitchakarn
Wanisa Punfa
Keywords: Biochemistry, Genetics and Molecular Biology;Medicine
Issue Date: 1-Jan-2015
Abstract: Anthocyanin, a phenolic compound, has been reported to have an anti-inflammatory effect against lipopolysaccharide (LPS) induced changes in immune cells. However, little is known about the molecular mechanisms underlying its anti-inflammatory effects. Few research studies have concerned the anti-inflammation properties of colored rice extract as a functional material. Therefore, the purpose of this study was to examine anti-inflammatory effects of the polar fraction of black rice whole grain extracts (BR-WG-P) that features a high anthocyanin content. Our results showed that BR-WG-P significantly inhibited LPS-induced proinflammatory mediators, including production of NO and expression of iNOS and COX-2. In addition, secretion of pro-inflammatory cytokines including TNF-a and IL-6 was also significantly inhibited. Moreover, BR-WG-P and anthocyanin inhibited NF-kB and AP-1 translocation into the nucleus. BR-WG-P also decreased the phosphorylation of ERK, p38 and JNK in a dose dependent manner. These results suggested that BR-WG-P might suppress LPS-induced inflammation via the inhibition of the MAPK signaling pathway leading to decrease of NF-kB and AP-1 translocation. All of these results indicate that BR-WG-P exhibits therapeutic potential associated with the anthocyanin content in the extract for treating inflammatory diseases associated with cancer.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84930714532&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/54157
ISSN: 15137368
Appears in Collections:CMUL: Journal Articles

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