Inhibition effects of Vitex rotundifolia on inflammatory gene expression in A549 human epithelial cells.
BACKGROUND
Vitex rotundifolia has long been used in traditional medicine to treat asthma and other allergic diseases.


OBJECTIVE
To evaluate the anti-inflammatory mechanisms of V rotundifolia in cultured A549 human alveolar epithelial cells.


METHODS
In the present study, A549 cells were stimulated with tumor necrosis factor alpha, interleukin 4, and interleukin 1beta to induce expression of chemokines and adhesion molecules involved in eosinophil chemotaxis. The anti-inflammatory effects of V rotundifolia on stimulated A549 cells were then evaluated by analyzing eotaxin secretion and eosinophil migration. In addition, the effects of V rotundifolia on gene expression profiles in stimulated A549 cells were evaluated by oligonucleotide microarray and real-time reverse transcription-polymerase chain reaction (RTRP).


RESULTS
The V rotundifolia-treated A549 cells had significantly suppressed eotaxin secretion and eosinophil migration in a dose-dependent manner. In addition, the results of the microarray analysis and RTRP revealed that inflammation-related genes and cell adhesion-related genes were down-regulated in V rotundifolia-treated A549 cells. Furthermore, several genes related to the mitogen-activated protein kinase pathway were down-regulated in V rotundifolia-treated A549 cells.


CONCLUSIONS
The mechanism responsible for the effects of V rotundifolia on A549 cells is closely associated with regulation of the mitogen-activated protein kinase pathway. Thus, V rotundifolia may be useful in the treatment of asthma and other allergic diseases.
Sohn
Sung-Hwa
SH
Department of Physiology, College of Oriental Medicine, Kyung Hee University, Seoul, Republic of Korea.
Ko
Eunjung
E
Oh
Bang-Gul
BG
Kim
Sung-Hoon
SH
Kim
Yangseok
Y
Shin
Minkyu
M
Hong
Moochang
M
Bae
Hyunsu
H
D015815:Cell Adhesion Molecules / Q000235:genetics; D002460:Cell Line; D002465:Cell Movement / Q000187:drug effects; D054413:Chemokine CCL11 / Q000378:metabolism; D018925:Chemokines / Q000235:genetics; D017077:Culture Media, Conditioned / Q000494:pharmacology; D016207:Cytokines / Q000235:genetics*; D015536:Down-Regulation / Q000235:genetics; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D004804:Eosinophils / Q000166:cytology / Q000187:drug effects; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism*; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000187:drug effects* / Q000235:genetics; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D053583:Interleukin-1beta / Q000494:pharmacology; D015847:Interleukin-4 / Q000494:pharmacology; D020935:MAP Kinase Signaling System / Q000235:genetics; D020411:Oligonucleotide Array Sequence Analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D015854:Up-Regulation / Q000235:genetics; D020950:Vitex / Q000737:chemistry*
C515456:CCL11 protein, human; D015815:Cell Adhesion Molecules; D054413:Chemokine CCL11; D018925:Chemokines; D017077:Culture Media, Conditioned; D016207:Cytokines; D004365:Drugs, Chinese Herbal; C508598:IL4 protein, human; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4