Date: June 2010

Journal: Archives of Pharmacal Research Volume 33, Issue 6, June 2010, Pages 843-851 , Doi: 10.1007/s12272-010-0606-6

2010 | Atractylodes japonica Koidzumi inhibits the production of proinflammatory cytokines through inhibition of the NF-κB/IκB signal pathway in HMC-1 human mast cells…

Hong, M.H.a, Kim, J.-H.b, Bae, H.c, Lee, N.-Y.d, Shin, Y.-C.a, Kim, S.-H.b, Ko, S.-G.abe


The rhizome of Atractylodes japonica Koidzumi (AJK) has been used in traditional medicine for treatment of arthritis, bronchitis and respiratory infectious disease, whereas its effects on inflammatory reactions have not been unknown recently. In this study, the effects of AJK on allergic inflammation and its signaling were investigated in the induced human mast cells and animal model. This study showed that ethanol extract of AJK interestingly suppressed the production and mRNA expression of TNF-α, IL-6 and IL-8, as important inflammatory cytokines. Furthermore, AJK inhibited the nuclear translocation of nuclear factor (NF)-κB through inhibition of the phosphorylation of IB-κ, which was additionally elucidated by NF-κB promoter-mediated luciferase activity. In addition, the phosphorylation of ERK was increased in pretreatment with AJK, whereas there was no change in JNK and p38 MAPK. However, AJK showed no effects on anti-DNP IgE-mediated in vivo PCA reaction and histamine release, as key events of mast cell-mediated immediate allergic reactions. These results suggest that AJK might be involved in not early-phase but transition to late-phase reactions of allergic inflammation and could modulate through other signal pathways. Taken together, AJK could be used as a treatment for mast cell mediated late-phase/chronic allergic inflammatory reactions. © 2010 The Pharmaceutical Society of Korea and Springer Netherlands.

Author keywords

Allergic inflammation; Atractylodes japonica Koidzumi; Human mast cells; NF-κB; Pro-inflammatory cytokine

Indexed keywords

EMTREE drug terms: antiinflammatory agent; Atractylode japonica koidzumi extract; I kappa B kinase alpha; immunoglobulin E; immunoglobulin enhancer binding protein; interleukin 6; interleukin 8; messenger RNA; mitogen activated protein kinase; mitogen activated protein kinase p38; plant extract; stress activated protein kinase; tumor necrosis factor alpha; unclassified drug

EMTREE medical terms: allergic reaction; animal cell; animal experiment; animal model; antiinflammatory activity; article; Atractylode japonica koidzumi; Atractylodes; cytokine production; cytotoxicity; drug effect; gene expression; high performance liquid chromatography; histamine release; human; human cell; immediate type hypersensitivity; inflammation; male; mast cell; nonhuman; passive skin anaphylaxis; protein phosphorylation; rat; signal transduction

MeSH: Animals; Anti-Inflammatory Agents; Atractylodes; Cell Line; Cell Survival; Cytokines; Gene Expression Regulation; Humans; I-kappa B Proteins; Lactones; Male; Mast Cells; Medicine, East Asian Traditional; NF-kappa B; Passive Cutaneous Anaphylaxis; Plant Extracts; Rats; Rats, Sprague-Dawley; Rhizome; RNA, Messenger; Sesquiterpenes; Signal Transduction
Medline is the source for the MeSH terms of this document.

Chemicals and CAS Registry Numbers: immunoglobulin E, 37341-29-0; interleukin 8, 114308-91-7; mitogen activated protein kinase, 142243-02-5; stress activated protein kinase, 155215-87-5;Anti-Inflammatory Agents; Cytokines; I-kappa B Proteins; Lactones; NF-kappa B; Plant Extracts; RNA, Messenger; Sesquiterpenes; atractylenolide III

ISSN: 02536269 CODEN: APHRDSource Type: Journal Original language: English
DOI: 10.1007/s12272-010-0606-6 PubMed ID: 20607488 Document Type: Article
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