Aromadendrin Inhibits Lipopolysaccharide-Induced Nuclear Translocation of NF-κB and Phosphorylation of JNK in RAW 264.7 Macrophage Cells

Aromadendrin Inhibits Lipopolysaccharide-Induced Nuclear Translocation of NF-κB and Phosphorylation of JNK in RAW 264.7 Macrophage Cells

Aromadendrin, a fl avonol, has been reported to possess a variety of pharmacological activities such as anti-infl ammatory, 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-infl ammatory mechanism of aromadedrin in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. Aromadendrin signifi cantly suppressed LPS-induced excessive production of pro-infl ammatory mediators such as nitric oxide (NO) and PGE2. In accordance, aromadendrin attenuated LPSinduced overexpression iNOS and COX-2. In addition, aromadendrin signifi cantly suppressed LPS-induced degradation of IκB,which sequesters NF-κB in cytoplasm, consequently inhibiting the nuclear translocation of pro-infl ammatory transcription factor NF-κB. To elucidate the underlying signaling mechanism of anti-infl ammatory activity of aromadendrin, MAPK signaling pathway was examined. Aromadendrin signifi cantly 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-infl ammatory activity through the suppression of nuclear translocation of NF-κB and phosphorylation of JNK in LPS-stimulated RAW 264.7 macrophage cells.

Aromadendrin, a fl avonol, has been reported to possess a variety of pharmacological activities such as anti-infl ammatory, 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-infl ammatory mechanism of aromadedrin in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. Aromadendrin signifi cantly suppressed LPS-induced excessive production of pro-infl ammatory mediators such as nitric oxide (NO) and PGE2. In accordance, aromadendrin attenuated LPSinduced overexpression iNOS and COX-2. In addition, aromadendrin signifi cantly suppressed LPS-induced degradation of IκB,which sequesters NF-κB in cytoplasm, consequently inhibiting the nuclear translocation of pro-infl ammatory transcription factor NF-κB. To elucidate the underlying signaling mechanism of anti-infl ammatory activity of aromadendrin, MAPK signaling pathway was examined. Aromadendrin signifi cantly 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-infl ammatory activity through the suppression of nuclear translocation of NF-κB and phosphorylation of JNK in LPS-stimulated RAW 264.7 macrophage cells.