Essential oil of Artemisia argyi suppresses inflammatory responses by inhibiting JAK/STATs activation

被引:68
作者
Chen, Lin-Lin [1 ]
Zhang, Hao-Jun [2 ]
Chao, Jung [3 ]
Liu, Jun-Feng [1 ]
机构
[1] Hubei Univ Chinese Med, Minist Educ, Key Lab Tradit Chinese Med Resource & Compound Pr, Wuhan 430065, Peoples R China
[2] China Japan Friendship Hosp, Dept Pharmacol, Beijing 100029, Peoples R China
[3] Natl Yang Ming Univ, Dept & Inst Pharmacol, Taipei 112, Taiwan
关键词
Artemisia argyi; Anti-inflammatory; JAK/STATs; NF-KAPPA-B; JAK-STAT PATHWAY; ANTIINFLAMMATORY ACTIVITIES; SIGNALING PATHWAYS; GENE-EXPRESSION; IN-VITRO; MACROPHAGES; MEDIATORS; FIBROBLASTS; ANTIOXIDANT;
D O I
10.1016/j.jep.2017.04.017
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Ethnopharmacological relevance: Artemisia argyi is a herbal medicine traditionally used in Asia for the treatment of bronchitis, dermatitis and arthritis. Recent studies revealed the anti-inflammatory effect of essential oil in this plant. However, the mechanisms underlying the therapeutic potential have not been well elucidated. The present study is aimed to verify its anti-inflammatory effect and investigate the probable mechanisms. Materials and methods: The essential oil from Artemisia argyi (AAEO) was initially tested against LPS-induced production of inflammatory mediators and cytokines in RAW264.7 macrophages. Protein and mRNA expressions of iNOS and COX-2 were determined by Western blotting and RT-PCR analysis, respectively. The effects on the activation of MAPK/NF-kappa B/AP-1 and JAK/STATs pathway were also investigated by western blot. Meanwhile, in vivo anti-inflammatory effect was examined by histologic and immunohistochemical analysis in TPA-induced mouse ear edema model. Results: The results of in vitro experiments showed that AAEO dose-dependently suppressed the release of pro inflammatory mediators (NO, PGE2 and ROS) and cytokines (TNF-alpha, IL-6, IFN-beta and MCP-1) in LPS-induced RAW264.7 macrophages. It down-regulated iNOS and COX-2 protein and mRNA expression but did not affect the activity of these two enzymes. AAEO significantly inhibited the phosphorylation of JAK2 and STAT1/3, but not the activation of MAPK and NF-kappa B cascades. In animal model, oral administration of AAEO significantly attenuated TPA-induced mouse ear edema and decreased the protein level of COX-2. Conclusion: AAEO suppresses inflammatory responses via down-regulation of the JAK/STATs signaling and ROS scavenging, which could contribute, at least in part, to the anti-inflammatory effect of AAEO.
引用
收藏
页码:107 / 117
页数:11
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