Publication: 1,5-Anhydro-d-fructose attenuates lipopolysaccharide-induced cytokine release via suppression of NF-κB p65 phosphorylation
Issued Date
2009-03-06
Resource Type
ISSN
10902104
0006291X
0006291X
Other identifier(s)
2-s2.0-60349098894
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Mahidol University
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SCOPUS
Bibliographic Citation
Biochemical and Biophysical Research Communications. Vol.380, No.2 (2009), 343-348
Suggested Citation
Xiaojie Meng, Ko ichi Kawahara, Yuko Nawa, Naoki Miura, Binita Shrestha, Salunya Tancharoen, Hisayo Sameshima, Teruto Hashiguchi, Ikuro Maruyama 1,5-Anhydro-d-fructose attenuates lipopolysaccharide-induced cytokine release via suppression of NF-κB p65 phosphorylation. Biochemical and Biophysical Research Communications. Vol.380, No.2 (2009), 343-348. doi:10.1016/j.bbrc.2009.01.084 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/27267
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Title
1,5-Anhydro-d-fructose attenuates lipopolysaccharide-induced cytokine release via suppression of NF-κB p65 phosphorylation
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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.