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Anti-allergic effects and mechanisms of action of the ethanolic extract of Angelica gigas in dinitrofluorobenzene-induced inflammation models

Authors
Joo, Seong SooPark, DongsunShin, SunheeJeon, Jeong HeeKim, Tae KyunChoi, Young JinLee, Sun HeeKim, Jeong SeonPark, Sung KyeongHwang, Bang YeonLee, Do IkKim, Yun-Bae
Issue Date
Sep-2010
Publisher
ELSEVIER SCIENCE BV
Keywords
Inflammation; Allergic dermatitis; Angelica gigas; 2,4-Dinitrofluorobenzene
Citation
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY, v.30, no.2, pp 127 - 133
Pages
7
Journal Title
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
Volume
30
Number
2
Start Page
127
End Page
133
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/22241
DOI
10.1016/j.etap.2010.04.007
ISSN
1382-6689
1872-7077
Abstract
To confirm the anti-allergic effects of the ethanolic extract of Angelica gigas (EAG), the levels of ear erythema, ear weight, vascular leakage, heamatology, tumor-necrosis factor-alpha, interleukin-6 and immunoglobulin E from mice sensitized with 2.4-dinitroflurorobenzene were examined. The results showed that EAG reduced ear erythema and ear weight, we also found that Evan's blue leakage decreased Furthermore, the levels of interleukin-6 and immunoglobulin E in the serum were significantly inhibited In RAW264.7 cells, EAG drastically inhibited the m RNA levels of inducible nitric oxide synthease, tumor-necrosis factor-alpha and macrophage inflammatory protein-1 beta, suggesting that EAG may inhibit the release of pro-inflammatory cytokines and acute neutrophilic inflammation Western blot analysis showed that EAG inhibited nuclear factor-kappa B- and extracelullar signal-regulated protein kinase-dependent inflammatory pathways Interestingly. EAG effectively inhibited the release of beta-hexosaminidase, a granule marker from mast cells Taken together, our results demonstrate that EAG inhibits focal and systemic inflammatory and allergic reactions, and holds great promise for the treatment of several inflammatory diseases. (C) 2010 Elsevier B V All rights reserved
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