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Root extract of Angelica reflexa BYLee reduces allergic lung inflammation by regulating Th2 cell activation
被引:2
|作者:
Kim, Sung Bae
[1
,2
]
Seo, Yun-Soo
[1
]
Kim, Hyo Seon
[1
]
Lee, A. Yeong
[1
]
Chun, Jin Mi
[1
]
Kim, Wook Jin
[1
]
Moon, Byeong Cheol
[1
]
Kwon, Bo-In
[3
,4
]
机构:
[1] Korea Inst Oriental Med, Herbal Med Resources Res Ctr, Naju Si 58245, Jeollanam Do, South Korea
[2] Korea Conform Labs KCL, Bio Technol Div, Incheon 21999, South Korea
[3] Sangji Univ, Coll Korean Med, Dept Pathol, Wonju 26339, Gangwon Do, South Korea
[4] Sangji Univ, Res Inst Korean Med, Wonju 26339, Gangwon Do, South Korea
基金:
新加坡国家研究基金会;
关键词:
Angelica reflexa BY Lee;
Asthma;
Th2;
cell;
Interferon regulatory factor 4;
Eosinophil;
D O I:
10.1016/j.jep.2020.113752
中图分类号:
Q94 [植物学];
学科分类号:
071001 ;
摘要:
Ethnopharmacological relevance: Traditionally, the roots of Angelica reflexa B.Y.Lee (AR) have been used to treat cough, phlegm, neuralgia, and arthralgia in Northeast Asia. Aim of the study: The anti-asthmatic effect of AR root extract (ARE) was determined using a murine airway allergic inflammation model and the primary T cell polarization assay. Materials and methods: To evaluate the anti-asthmatic effect of ARE, inflammatory cell infiltration was determined histologically and inflammatory mediators were measured in bronchoalveolar lavage fluid (BALF). Furthermore, the effects of AREs on Th2 cell differentiation and activation were determined by western blotting and flow cytometry. Results: Asthmatic phenotypes were alleviated by ARE treatment, which reduced mucus production, inflammatory cell infiltration (especially eosinophilia), and type 2 cytokine levels in BALF. ARE administration to mice reduced the number of activated Th2 (CD4(+)CD25(+)) cells and level of GATA3 in the lungs. Furthermore, ARE treatment inhibited the differentiation of Th2 cells in primary cell culture systems via interferon regulatory factor 4 (IRF4) signaling. Conclusions: Our findings indicate that the anti-asthmatic effect of AREs is mediated by the reduction in Th2 cell activation by regulating IRF4.
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