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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/27267
Title: 1,5-Anhydro-d-fructose attenuates lipopolysaccharide-induced cytokine release via suppression of NF-κB p65 phosphorylation
Authors: Xiaojie Meng
Ko ichi Kawahara
Yuko Nawa
Naoki Miura
Binita Shrestha
Salunya Tancharoen
Hisayo Sameshima
Teruto Hashiguchi
Ikuro Maruyama
Department of Laboratory and Vascular Medicine
Veterinary Teaching Hospital
Mahidol University
Keywords: Biochemistry, Genetics and Molecular Biology
Issue Date: 6-Mar-2009
Citation: Biochemical and Biophysical Research Communications. Vol.380, No.2 (2009), 343-348
Abstract: Lipopolysaccharide (LPS) stimulates macrophages by activating NF-κB, which contributes to the release of tumor necrosis factor (TNF)-α and interleukin (IL)-6. 1,5-anhydro-d-fructose (1,5-AF), a monosaccharide formed from starch and glycogen, exhibits anti-oxidant activity and enhances insulin secretion. This study examined the effects of 1,5-AF on LPS-induced inflammatory reactions and elucidated its molecular mechanisms. Before LPS challenge, mice were pretreated with 1,5-AF (38.5 mg/kg). We found that 1,5-AF pretreatment attenuated cytokine release into the serum, including TNF-α, IL-6 and macrophage chemoattractant protein (MCP)-1. Furthermore, pretreatment with 1,5-AF (500 μg/ml) attenuated cytokine release, and 1,5-AF directly inhibited the nuclear translocalization of the NF-κB p65 subunit in LPS-stimulated murine macrophage-like RAW264.7 cells. This inhibition was responsible for decreased LPS-induced phosphorylation on Ser536 of the NF-κB p65 subunit, which is a posttranslational modification involved in the non-canonical pathway. Collectively, these findings indicate that the anti-inflammatory activity of 1,5-AF occurs via inactivation of NF-κB. © 2009 Elsevier Inc. All rights reserved.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=60349098894&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/27267
ISSN: 10902104
0006291X
Appears in Collections:Scopus 2006-2010

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