当前位置： SCI文献检索 > JOURNAL OF ETHNOPHARMACOLOGY期刊下所有文献 > Panax quinquefolium saponins inhibited immune maturation of human monocyte-derived dendritic cells via blocking nuclear factor-κB pathway.

Panax quinquefolium saponins inhibited immune maturation of human monocyte-derived dendritic cells via blocking nuclear factor-κB pathway.

Abstract：

ETHNOPHARMACOLOGICAL RELEVANCE:Panax quinquefolium saponins (PQS), a water-soluble antioxidant extracted from a natural herb, radix panacis quinquefolii (American Ginseng), has yielded encouraging results in the treatment of atherosclerotic diseases. However, the underlying mechanisms remain unclear. Here, we tested the hypothesis that the anti-atherosclerotic effect of PQS might be mediated by suppressing human monocyte-derived dendritic cells (DCs) maturation. MATERIALS AND METHODS:DCs were derived by incubating purified human monocytes with granulocyte macrophage colony stimulating factor (GM-CSF) and IL-4. DCs were pre-incubated with or without PQS and stimulated by oxidized low density lipoprotein (ox-LDL). Expression of DCs membrane molecules (CD40, CD86, CD1a, HLA-DR) and endocytotic ability were analyzed by FACS, cytokines (IL-12 and TNF-α) were measured by ELISA. Nuclear factor (NF)-κB signaling pathway was determined by Western blotting, and RT-PCR. NF-κB activation was quantified by ELISA. RESULTS:PQS reduced ox-LDL induced immunophenotypic expressions (CD40, CD1a, CD86, and HLA-DR) and cytokine secretions (IL-12 and TNF-α), and improved endocytotic ability of DCs. These above phenomena were accompanied by decreased protein expression and binding activity of nuclear localized c-Rel subunit. CONCLUSIONS:Our study suggested that PQS inhibited ox-LDL induced immune maturation of DCs in vitro, which might be in part mediated by NF-κB signal transduction pathway.

journal_name

J Ethnopharmacol

journal_title

Journal of ethnopharmacology

authors

Liu H,Shi D,Wang W,Zhang C,Fu M,Ge J

doi

10.1016/j.jep.2012.03.029

subject

Has Abstract

pub_date

2012-06-14 00:00:00

pages

982-8

issue

3

eissn

0378-8741

issn

1872-7573

pii

S0378-8741(12)00189-4

journal_volume

141

pub_type

杂志文章

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