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Year : 2016  |  Volume : 12  |  Issue : 48  |  Page : 295-301

Oryza sativa (Rice) hull extract inhibits lipopolysaccharide-induced inflammatory response in RAW264.7 macrophages by suppressing extracellular signal-regulated kinase, c-jun n-terminal kinase, and nuclear factor-κb activation

1 Research Group of Nutraceuticals for Metabolic Syndrome, Korea Food Research Institute, Gyeonggi; Division of Food Biotechnology, University of Science and Technology, Daejeon, Republic of Korea
2 Research Group of Nutraceuticals for Metabolic Syndrome, Korea Food Research Institute, Gyeonggi, Republic of Korea

Correspondence Address:
Dr. Yoonsook Kim
Research group of nutraceuticals for metabolic syndrome, Korea Food Research Institute Gyeonggi
Republic of Korea
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0973-1296.192198

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Background: Rice (Oryza sativa ) is a major cereal crop in many Asian countries and an important staple food source. Rice hulls have been reported to possess antioxidant activities. Materials and Methods: In this study, we evaluated the antiinflammatory effects of rice hull extract and associated signal transduction mechanisms in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Results: We found that rice hull extract inhibited nitric oxide (NO) and prostaglandin E2 by suppressing the expression of inducible NO synthase and cyclooxygenase-2, respectively. The release of interleukin-1β and tumor necrosis factor-α was also reduced in a dose-dependent manner. Furthermore, rice hull extract attenuated the activation of nuclear factor-kappa B (NF-κB), as well as the phosphorylation of mitogen-activated protein kinases, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK), in LPS-stimulated RAW264.7 cells. Conclusion: This suggests that rice hull extract decreases the production of inflammatory mediators by downregulating ERK and JNK and the NF-κB signal pathway in RAW 264.7 cells. Abbreviation used: COX-2: cyclooxygenase-2, ERK: extracellular signal-regulated kinase, IκB: inhibitory kappa B, IL-1β: interleukin-1β, iNOS: inducible NO synthase, JNK: c-Jun N-terminal kinase, LPS: lipopolysaccharide, MAPKs: mitogen-activated protein kinases, NF-κB: nuclear factor-κB, NO: nitric oxide, PGE2: prostaglandin E2, RHE: rice hull extract, ROS: reactive oxygen species, TNF-α: tumor necrosis factor-α

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