Journal
BIOMOLECULES & THERAPEUTICS
Volume 21, Issue 3, Pages 216-221Publisher
KOREAN SOC APPLIED PHARMACOLOGY
DOI: 10.4062/biomolther.2013.023
Keywords
Aromadendrin; COX-2; iNOS; JNK; Lipopolysaccharide; NF-kappa B; RAW 264.7 cells
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Aromadendrin, a flavonol, has been reported to possess a variety of pharmacological activities such as anti-inflammatory, antioxidant, and anti-diabetic properties. However, the underlying mechanism by which aromadendrin exerts its biological activity has not been extensively demonstrated. The objective of this study is to elucidate the anti-inflammatory mechanism of aromadedrin in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. Aromadendrin significantly suppressed LPS-induced excessive production of pro-inflammatory mediators such as nitric oxide (NO) and PGE(2). In accordance, aromadendrin attenuated LPS-induced overexpression iNOS and COX-2. In addition, aromadendrin significantly suppressed LPS-induced degradation of I kappa B, which sequesters NF-kappa B in cytoplasm, consequently inhibiting the nuclear translocation of pro-inflammatory transcription factor NF-kappa B. To elucidate the underlying signaling mechanism of anti-inflammatory activity of aromadendrin, MAPK signaling pathway was examined. Aromadendrin significantly attenuated LPS-induced activation of JNK, but not ERK and p38, in a concentration-dependent manner. Taken together, the present study clearly demonstrates that aromadendrin exhibits anti-inflammatory activity through the suppression of nuclear translocation of NF-kappa B and phosphorylation of JNK in LPS-stimulated RAW 264.7 macrophage cells.
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