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Allium hookeri root extract regulates asthmatic changes through immunological modulation of Th1/Th2-related factors in an ovalbumin-induced asthma mouse modelopen access

Authors
Bok, So-HyeonSeo, Ji-HyeBae, Chun-SikKang, BossngCho, Seung SikPark, Dae-Hun
Issue Date
Oct-2019
Publisher
SPANDIDOS PUBL LTD
Keywords
Allium hookeri; ovalbumin-induced asthma; CD68; MHC class II; TNF-alpha
Citation
MOLECULAR MEDICINE REPORTS, v.20, no.4, pp.3215 - 3223
Indexed
SCIE
SCOPUS
Journal Title
MOLECULAR MEDICINE REPORTS
Volume
20
Number
4
Start Page
3215
End Page
3223
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/147083
DOI
10.3892/mmr.2019.10560
ISSN
1791-2997
Abstract
In 2013, WHO estimated that approximately 235 million people suffered from asthma worldwide. Asthma is a hyper responsive disorder, which is related to an imbalance between the T-helper type 1 and 2 cells (henceforth, Th1 and Th2, respectively). Allium hookeri is a plant that is widely used for culinary purposes and also in traditional Asian medicine. The present study was conducted to elucidate the anti-asthmatic effects and mechanism of action of A. hookeri root extracts (AHRE) in an ovalbumin (OVA)-induced asthma mouse model. The mice were divided into five groups, namely, the control, the OVA-treated group, the dexamethasone-treated group, the 30 mg/kg AHRE-treated group, and the 300 mg/kg AHRE-treated group. The total WBC count and the differential cell count in the bronchoalveolar fluid, the level of serum IgE, the histopathological changes in the lung, and changes in the cell surface molecules, the asthma-related cytokine levels, and Th cell transcription factors were evaluated. AHRE significantly ameliorated asthmatic changes, such as the total WBC count, eosinophil count, and the level of IgE; in addition, it reduced mucus hypersecretion, epithelial hyperplasia, and eosinophil infiltration in the lungs. AHRE significantly inhibited the expression of CD68(+) cells and MHC class II+ molecules, Th1 cell transcription factor (T-bet) activation, Th2 cell transcription factor (GATA-3) activation, and TNF-alpha in the lung tissue. Furthermore, it suppressed cell surface molecules, such as CD4(+)and CD8(+); Th1-related cytokines, such as IFN-gamma and IL-12p40; Th2-related cytokines, such as IL-4 and IL-5; and Th17-related cytokines, such as IL-6 and TNF-alpha, in a dose-dependent manner. Thus, AHRE may be considered a promising anti-asthmatic drug.
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