Effect of Caffeic Acid Phenethyl Ester on Lipopolysaccharide-induced Murine Macrophage Activation
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Background: Caffeic acid phenethyl ester (CAPE) is an active component of propolis and is known to have anti-inflammatory properties. This study was performed to evaluate the effects of CAPE on lipopolysaccharide (LPS)-induced murine macrophage activation. Methods: Raw 264.7 cells were incubated with varying concentrations of CAPE with or without LPS. The production of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β and macrophage inflammatory protein-2 (MIP-2) and activation of extracellular signal-regulated kinases 1/2 (ERK1/2), c-Jun amino terminal kinases (JNK) and p38 were measured. Results: CAPE inhibited the production of TNF-α, IL-1β and MIP-2 and attenuated phosphorylation levels of ERK1/2 and p38, but not JNK in RAW264.7 cells stimulated with LPS. Conclusions: CAPE can attenuate LPS-induced macrophage responses and we suggest that these effects may play an important role in modulating macrophage-mediated inflammatory responses in vivo.
Abstract
Background: Caffeic acid phenethyl ester (CAPE) is an active component of propolis and is known to have anti-inflammatory properties. This study was performed to evaluate the effects of CAPE on lipopolysaccharide (LPS)-induced murine macrophage activation. Methods: Raw 264.7 cells were incubated with varying concentrations of CAPE with or without LPS. The production of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β and macrophage inflammatory protein-2 (MIP-2) and activation of extracellular signal-regulated kinases 1/2 (ERK1/2), c-Jun amino terminal kinases (JNK) and p38 were measured. Results: CAPE inhibited the production of TNF-α, IL-1β and MIP-2 and attenuated phosphorylation levels of ERK1/2 and p38, but not JNK in RAW264.7 cells stimulated with LPS. Conclusions: CAPE can attenuate LPS-induced macrophage responses and we suggest that these effects may play an important role in modulating macrophage-mediated inflammatory responses in vivo.
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