Inhibition effects of Moutan Cortex Radicis on secretion of eotaxin in A549 human epithelial cells and eosinophil migration.
Eosinophils have been implicated in a broad range of diseases, most notably allergic conditions (e.g. asthma, rhinitis and atopic dermatitis) and inflammatory diseases. These diseases are characterized by an accumulation of eosinophils in the tissue. Defining the mechanisms that control eosinophil recruitment is fundamental to understanding how these diseases progress and may identify a novel target for drug therapy. Eotaxin is a potent eosinophil-specific chemokine that is released in the respiratory epithelium after allergic stimulation.


OBJECTIVE
In this study, we determined whether Moutan Cortex Radicis (MCR), a plant extract, effects eotaxin secretion from A549 epithelial cells and eosinophil chemotaxis, and then examined the mechanism involved.


METHODS
Prior to assaying MCR's effects, A549 cells were stimulated with tumor necrosis factor-alpha (TNF-alpha), interleukin-4 (IL-4) and IL-1beta to induce expression of chemokines and adhesion molecules involved in eosinophil chemotaxis. In the presence of MCR, eotaxin, regulated on activation in normal T cells expressed and secreted (RANTES), IL-8, IL-16, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) transcripts were quantitated by real-time RT-PCR.


RESULTS
As a result, 0.01, 1, and 100 microg/ml of MCR treatments reduced eotaxin expression significantly and 0.01, 0.1, 1, 10, and 100 microg/ml of MCR reduced significantly eotaxin secretion. In addition, MCR treatment significantly inhibited eosinophil migration toward A549 medium. And 100 microg/ml of MCR suppressed the activated of nuclear factor (NF)-kappaB.


CONCLUSIONS
These findings indicate that suppressed eotaxin secretion by MCR treatment is due to the inhibition of NF-kappaB activation. Therefore, MCR might be of therapeutic value in treating asthma.
Kim
Jinju
J
Department of Oriental Physiology, College of Pharmacy, Kyung Hee University, #1 Hoeki-dong Dongdaemoon-gu, Seoul 130-701, Republic of Korea.
Lee
Heekyung
H
Lee
Youngseop
Y
Oh
Bang-Gul
BG
Cho
Chongwoon
C
Kim
Yangseok
Y
Shin
Minkyu
M
Hong
Moochang
M
Jung
Sung-Ki
SK
Bae
Hyunsu
H
D015153:Blotting, Western; D002465:Cell Movement / Q000187:drug effects*; D002467:Cell Nucleus / Q000187:drug effects / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D018946:Chemokine CCL5 / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism*; D002634:Chemotaxis, Leukocyte / Q000187:drug effects; D002851:Chromatography, High Pressure Liquid; D016207:Cytokines / Q000378:metabolism; D018076:DNA, Complementary / Q000096:biosynthesis; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils / Q000187:drug effects*; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D053583:Interleukin-1beta / Q000037:antagonists & inhibitors / Q000494:pharmacology; D015847:Interleukin-4 / Q000037:antagonists & inhibitors / Q000494:pharmacology; D029596:Paeonia; D012333:RNA, Messenger / Q000096:biosynthesis / Q000302:isolation & purification; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000494:pharmacology
D018946:Chemokine CCL5; D018925:Chemokines; D016207:Cytokines; D018076:DNA, Complementary; D004365:Drugs, Chinese Herbal; D053583:Interleukin-1beta; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; C038881:moutan cortex; D015847:Interleukin-4