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Mungbean seed coat water extract inhibits inflammation in LPS-induced acute liver injury mice and LPS-stimulated RAW 246.7 macrophages via the inhibition of TAK1/IκBα/NF-κB

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Abstract

Inflammation plays an important role in pathogenesis and progression of many chronic diseases. Although, anti-inflammatory activities of mungbean have been suggested, the underlying mechanism have not been fully understood. The present study aimed to reveal the anti-inflammatory effects of mungbean seed coat water extract (MSWE) in lipopolysaccharide (LPS)-stimulated inflammation in RAW 246.7 macrophages and LPS-induced acute liver injury mice. MSWE pretreatment downregulated the elevated expression of inflammatory markers induced by LPS in the transcriptional and protein level. MSWE inhibited NF-κB activation through the suppression of phosphorylated p65 subunit, IκBα degradation, and transforming growth factor-β-activated kinases 1 (TAK1) phosphorylation in LPS-stimulated RAW 246.7 cells. Vitexin, the major flavonoid in MSWE showed similar effects. In in vivo experiments, we found that oral administration of MSWE downregulated iNOS expression in LPS-induced acute liver injury mice. The mRNA expression of inflammatory markers and macrophage infiltration was also decreased in the livers. Collectively, MSWE exerts anti-inflammatory role, in part possibly through its active compound vitexin, by inhibiting NF-κB activation via inhibition of TAK1 phosphorylation and IκBα degradation. This suggests that MSWE is beneficial to combat various inflammatory diseases.

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Acknowledgements

This work was supported by Grant-in-Aid for International Cooperative Research, Graduate School of Integrated Sciences for Life, Hiroshima University, Japan.

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Correspondence to Sudathip Sae-tan or Noriyuki Yanaka.

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Sae-tan, S., Kumrungsee, T. & Yanaka, N. Mungbean seed coat water extract inhibits inflammation in LPS-induced acute liver injury mice and LPS-stimulated RAW 246.7 macrophages via the inhibition of TAK1/IκBα/NF-κB. J Food Sci Technol 57, 2659–2668 (2020). https://doi.org/10.1007/s13197-020-04302-y

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