Autor: |
Yin, Hong Hua, Cho, Byoung Ok, Jang, Seon Il, Park, Sang Hyun, Byun, Eui Baek, Ha, Hun Yong |
Předmět: |
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Zdroj: |
Bioscience, Biotechnology & Biochemistry; Aug2016, Vol. 80 Issue 8, p1520-1530, 11p |
Abstrakt: |
Diospyros lotusis traditionally used for the treatment of diabetes, diarrhea, tumor, and hypertension. The purpose of this study was to investigate the anti-inflammatory effect and underlying molecular mechanisms of myricetin in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Myricetin dose-dependently suppressed the production of pro-inflammatory mediators (NO, iNOS, PGE2, and COX-2) in LPS-stimulated RAW264.7 macrophages. Myricetin administration decreased the production of NO, iNOS, TNF-α, IL-6, and IL-12 in mice. Myricetin decreased NF-κB activation by suppressing the degradation of IκBα, nuclear translocation of p65 subunit of NF-κB, and NF-κB DNA binding activity in LPS-stimulated RAW264.7 macrophages. Moreover, myricetin attenuated the phosphorylation of STAT1 and the production of IFN-β in LPS-stimulated RAW264.7 macrophages. Furthermore, myricetin induced the expression of HO-1 through Nrf2 translocation. In conclusion, these results suggest that myricetin inhibits the production of pro-inflammatory mediators through the suppression of NF-κB and STAT1 activation and induction of Nrf2-mediated HO-1 expression in LPS-stimulated RAW264.7 macrophages. This study has elucidated the anti-inflammatory effects of myricetin inin vitroandin vivo. [ABSTRACT FROM PUBLISHER] |
Databáze: |
Complementary Index |
Externí odkaz: |
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