Anti-inflammatory effects of Artemisia scoparia and its active constituent, 3,5-dicaffeoyl-epi-quinic acid against activated mast cells

被引:28
作者
Nam, Sun-Young [1 ]
Han, Na-Ra [1 ]
Rah, So-Young [2 ]
Seo, Youngwan [3 ]
Kim, Hyung-Min [1 ]
Jeong, Hyun-Ja [4 ]
机构
[1] Kyung Hee Univ, Dept Pharmacol, Coll Korean Med, 26 Kyungheedae Ro, Seoul 02447, South Korea
[2] Chonbuk Natl Univ, Dept Biochem, Jeonju, South Korea
[3] Korea Maritime Univ, Div Marine Environm & Biosci, Busan, South Korea
[4] Hoseo Univ, Dept Food Sci & Technol, 20,Hoseo Ro 79beon Gil, Baebang Eup 31499, Asan, South Korea
基金
新加坡国家研究基金会;
关键词
Artemisia scoparia Waldst. et Kit; 3,5-dicaffeoyl-epiquinic acid; mast cell; thymic stromal lymphopoietin; caspase-1; THYMIC STROMAL LYMPHOPOIETIN; KAPPA-B ACTIVATION; AIRWAY INFLAMMATION; IN-VITRO; ROLES; INHIBITION; EXPRESSION; MDM2; MICE;
D O I
10.1080/08923973.2017.1405438
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Objectives: Artemisia scoparia Waldst. et Kit. (AS) has been used to treat inflammation, urticaria and hepatitis. However, the scientific studies of AS and its active compound for inflammatory reactions in activated human mast cell line, HMC-1 cells have not yet been elucidated. Materials and methods: Here, we isolated 3,5-dicaffeoyl-epi-quinic acid (DEQA) from AS butanol fraction. The anti-inflammatory effect of AS and its new active compound, DEQA was examined in HMC-1 cells by studying the following markers: phorbol 12-myristate 13-acetate and calcium ionophore A23187 (PMACI)-induced thymic stromal lymphopoietin (TSLP), tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta and IL-6 secretion and mRNA expression by ELISA and RT-PCR, respectively. Furthermore, mechanism related to anti-inflammatory was examined by Western blotting. Results: We reported that AS and its new active compound, DEQA significantly reduced TSLP, TNF-alpha, IL-1 beta and IL-6 production levels through the reduction of caspase-1 activity. The mRNA expression of these inflammatory cytokine was also reduced via blocking nuclear factor-kappa B nuclear translocation by AS and DEQA. In addition, AS significantly reduced phosphorylated-c-Jun N-terminal kinase level and DEQA significantly reduced both phosphorylated-c-Jun N-terminal kinase and -p38 mitogen-activated protein kinase levels. Conclusions: Therefore, these results indicated that AS and its active compound, DEQA may improve mast cell-mediated inflammatory diseases.
引用
收藏
页码:52 / 58
页数:7
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