Atractylodes japonica Koidzumi Inhibits the Production of Pro-inflammatory Cytokines through Inhibition of the NF-κB/IκB Signal Pathway in HMC-1 Human Mast Cells

被引:31
作者
Hong, Myung Hee [1 ]
Kim, Jeong-Hyun [2 ]
Bae, Hyunsu [3 ]
Lee, Na-Youn [4 ]
Shin, Yong-Cheol [1 ]
Kim, Sung-Hoon [2 ]
Ko, Seong-Gyu [1 ,2 ,5 ]
机构
[1] Kyung Hee Univ, Dept Prevent Med, Coll Oriental Med, Seoul 130701, South Korea
[2] Kyung Hee Univ, Canc Prevent Mat Dev Res Ctr, Coll Oriental Med, Seoul 130701, South Korea
[3] Kyung Hee Univ, Dept Physiol, Coll Oriental Med, Seoul 130701, South Korea
[4] Kyung Hee Univ, Purimed R&D Inst, Seoul 130701, South Korea
[5] Univ Texas MD Anderson Canc Ctr, Dept Expt Therapeut, Houston, TX 77030 USA
关键词
Atractylodes japonica Koidzumi; Allergic inflammation; Human mast cells; NF-kappa B; Pro-inflammatory cytokine; PASSIVE CUTANEOUS ANAPHYLAXIS; TNF-ALPHA; ACTIVATION;
D O I
10.1007/s12272-010-0606-6
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
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-alpha, IL-6 and IL-8, as important inflammatory cytokines. Furthermore. AJK inhibited the nuclear translocation of nuclear factor (NF)-kappa B through inhibition of the phosphorylation of I kappa B-alpha, which was additionally elucidated by NF-kappa B 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.
引用
收藏
页码:843 / 851
页数:9
相关论文
共 30 条
[11]   Integrated signalling pathways for mast-cell activation [J].
Gilfillan, AM ;
Tkaczyk, C .
NATURE REVIEWS IMMUNOLOGY, 2006, 6 (03) :218-230
[12]   PURIFICATION OF RAT CUTANEOUS MAST-CELLS WITH PERCOLL DENSITY CENTRIFUGATION [J].
HACHISUKA, H ;
KUSUHARA, M ;
HIGUCHI, M ;
OKUBO, K ;
SASAI, Y .
ARCHIVES OF DERMATOLOGICAL RESEARCH, 1988, 280 (06) :358-362
[13]   Prevention of arthritic inflammation using an oriental herbal combination BDX-1 isolated from Achyranthes bidentata and Atractylodes japonica [J].
Han, SB ;
Lee, CW ;
Yoon, YD ;
Lee, JH ;
Kang, JS ;
Lee, KH ;
Yoon, WK ;
Lee, K ;
Park, SK ;
Kim, HM .
ARCHIVES OF PHARMACAL RESEARCH, 2005, 28 (08) :902-908
[14]   PRODUCTION OF PASSIVE CUTANEOUS ANAPHYLAXIS (PCA) AND REVERSED PCA BY RAT IGE ANTIBODY IN THE MOUSE [J].
HARADA, M ;
NAGATA, M ;
TAKEUCHI, M .
EXPERIENTIA, 1988, 44 (05) :459-462
[15]   Atractylodes japonica suppresses lipopolysaccharide-stimulated expressions of inducible nitric oxide synthase and cyclooxygenase-2 in RAW 264.7 macrophages [J].
Jang, MH ;
Shin, MC ;
Kim, YJ ;
Kim, CJ ;
Kim, Y ;
Kim, EH .
BIOLOGICAL & PHARMACEUTICAL BULLETIN, 2004, 27 (03) :324-327
[16]  
Jobin C, 1999, J IMMUNOL, V163, P3474
[17]   Phosphorylation meets ubiquitination:: The control of NF-κB activity [J].
Karin, M ;
Ben-Neriah, Y .
ANNUAL REVIEW OF IMMUNOLOGY, 2000, 18 :621-+
[18]   Cheongyeolsaseuptang inhibits production of TNF-α, IL-6 and IL-8 as well as NF-κB activation in human mast cells [J].
Kim, SJ ;
Lee, EJ ;
Song, YS ;
Jeong, HJ ;
Lee, KM ;
Kim, HR ;
Chae, HJ ;
Shin, TY ;
Kim, YK ;
Hong, SH ;
Kim, HM .
JOURNAL OF ETHNOPHARMACOLOGY, 2005, 97 (01) :83-88
[19]   Sounding the alarm: Protein kinase cascades activated by stress and inflammation [J].
Kyriakis, JM ;
Avruch, J .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (40) :24313-24316
[20]   Atractylenolide I and atractylenolide III inhibit lipopolysaccharide-induced TNF-α and NO production in macrophages [J].
Li, Cui-qin ;
He, Lang-Chong ;
Jin, Ju-qing .
PHYTOTHERAPY RESEARCH, 2007, 21 (04) :347-353