These authors contributed equally to this work.
Piperine Inhibits Lipopolysaccharide-induced Maturation of Bone-marrow-derived Dendritic Cells Through Inhibition of ERK and JNK Activation
Article first published online: 19 MAR 2012
Copyright © 2012 John Wiley & Sons, Ltd.
Volume 26, Issue 12, pages 1893–1897, December 2012
How to Cite
Bae, G.-S., Kim, J.-J., Park, K.-C., Koo, B. S., Jo, I.-J., Choi, S. B., Lee, C. H., Jung, W.-S., Cho, J.-H., Hong, S.-H., Song, H.-J., Shin, Y. K. and Park, S.-J. (2012), Piperine Inhibits Lipopolysaccharide-induced Maturation of Bone-marrow-derived Dendritic Cells Through Inhibition of ERK and JNK Activation. Phytother. Res., 26: 1893–1897. doi: 10.1002/ptr.4649
- Issue published online: 11 DEC 2012
- Article first published online: 19 MAR 2012
- dendritic cells;
Piperine, one of the main components of Piper longum Linn. and P. nigrum Linn., is a plant alkaloid with a long history of medicinal use. Piperine has been shown to modulate the immune response, but the mechanism underlying this modulation remains unknown. Here, we examined the effects of piperine on lipopolysaccharide (LPS)-induced inflammatory responses in bone-marrow-derived dendritic cells (BMDCs). Piperine significantly inhibited the expression of major histocompatibility complex class II, CD40 and CD86 in BMDCs in a dose-dependent manner. Furthermore, piperine treatment led to an increase in fluorescein-isothiocyanate–dextran uptake in LPS-treated dendritic cells and inhibited the production of tumour necrosis factor alpha and interleukin (IL)-12, but not IL-6. The inhibitory effects of piperine were mediated via suppression of extracellular signal-regulated kinases and c-Jun N-terminal kinases activation, but not p38 or nuclear factor-κB activation. These findings provide insight into the immunopharmacological role of piperine. Copyright © 2012 John Wiley & Sons, Ltd.