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Piperine Inhibits Lipopolysaccharide‐induced Maturation of Bone‐marrow‐derived Dendritic Cells Through Inhibition of ERK and JNK Activation
Author(s) -
Bae GiSang,
Kim JongJin,
Park KyoungChel,
Koo Bon Soon,
Jo IlJoo,
Choi Sun Bok,
Lee Chang Hyuk,
Jung WonSeok,
Cho JungHee,
Hong SeungHeon,
Song HoJoon,
Shin Yong Kook,
Park SungJoo
Publication year - 2012
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.4649
Subject(s) - piperine , lipopolysaccharide , fluorescein isothiocyanate , mapk/erk pathway , p38 mitogen activated protein kinases , pharmacology , chemistry , tumor necrosis factor alpha , kinase , biology , immunology , biochemistry , physics , quantum mechanics , fluorescence
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.