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Inhibition of lipopolysaccharide‐induced inflammatory responses by 1′‐acetoxychavicol acetate
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- Guang Han Ong
- Laboratory of Molecular Immunobiology, Division of Biological Science, Graduate School of Science and Technology Nara Institute of Science and Technology (NAIST) Ikoma Nara Japan
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- Daisuke Ori
- Laboratory of Molecular Immunobiology, Division of Biological Science, Graduate School of Science and Technology Nara Institute of Science and Technology (NAIST) Ikoma Nara Japan
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- Takumi Kawasaki
- Laboratory of Molecular Immunobiology, Division of Biological Science, Graduate School of Science and Technology Nara Institute of Science and Technology (NAIST) Ikoma Nara Japan
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- Taro Kawai
- Laboratory of Molecular Immunobiology, Division of Biological Science, Graduate School of Science and Technology Nara Institute of Science and Technology (NAIST) Ikoma Nara Japan
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Description
<jats:title>Abstract</jats:title><jats:p>Lipopolysaccharide on gram negative bacteria can be detected by Toll‐like receptor 4 (TLR4) to elicit a series of innate immune responses, leading to inflammation to eliminate the targeted pathogen. However, dysregulation in the responses results in excessive inflammation. The 1′‐acetoxychavicol acetate (ACA) is a bioactive compound originated from <jats:italic>Alpinia</jats:italic> species known to have anti‐inflammatory and apoptosis‐inducing properties. Here, we found that ACA inhibits lipopolysaccharide‐induced expression and production of proinflammatory cytokines such as interleukin 6 and TNFα by macrophages. ACA suppresses the activation of NF‐κB and MAP kinases in TLR4 signaling. Moreover, ACA also inhibits TLR4‐mediated induction of type I interferon by suppressing IRF3 activation. In lipopolysaccharide‐challenged mice, ACA treatment successfully increased the survival of mice and alleviated inflammation in the lung. Thus, ACA is a potential anti‐inflammatory agent to regulate excessive inflammation.</jats:p>
Journal
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- Genes to Cells
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Genes to Cells 27 (7), 482-492, 2022-05-08
Wiley
