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Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Biomol+Ther+(Seoul) 2015 ; 23 (5): 414-20 Nephropedia Template TP
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Fisetin Suppresses Macrophage-Mediated Inflammatory Responses by Blockade of Src and Syk #MMPMID26336580
Kim JH; Kim MY; Kim JH; Cho JY
Biomol Ther (Seoul) 2015[Sep]; 23 (5): 414-20 PMID26336580show ga
Flavonoids, such as fisetin (3,7,3?,4?-tetrahydroxyflavone), are plant secondary metabolites. It has been reported that fisetin is able to perform numerous pharmacological roles including anti-inflammatory, anti-microbial, and anti-cancer activities; however, the exact anti-inflammatory mechanism of fisetin is not understood. In this study, the pharmacological action modes of fisetin in lipopolysaccharide (LPS)-stimulated macrophage-like cells were elucidated by using immunoblotting analysis, kinase assays, and an overexpression strategy. Fisetin diminished the release of nitric oxide (NO) and reduced the mRNA levels of inducible NO synthase (iNOS), tumor necrosis factor (TNF)-?, and cyclooxygenase (COX)-2 in LPS-stimulated RAW264.7 cells without displaying cytotoxicity. This compound also blocked the nuclear translocation of p65/nuclear factor (NF)-?B. In agreement, the upstream phosphorylation events for NF-?B activation, composed of Src, Syk, and I?B?, were also reduced by fisetin. The phospho-Src level, triggered by overexpression of wild-type Src, was also inhibited by fisetin. Therefore, these results strongly suggest that fisetin can be considered a bioactive immunomodulatory compound with anti-inflammatory properties through suppression of Src and Syk activities.