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

• Published in: Journal of ethnopharmacology 2017-05, Vol.204, p.107-117
• Main Authors: Chen, Lin-Lin, Zhang, Hao-Jun, Chao, Jung, Liu, Jun-Feng
• Format: Article
• Language: English
• Subjects: Animals; Anti-inflammatory; Anti-Inflammatory Agents - pharmacology; Anti-Inflammatory Agents - therapeutic use; Artemisia; Artemisia argyi; Cyclooxygenase 2 - genetics; Cyclooxygenase 2 - metabolism; Cytokines - metabolism; Dinoprostone - metabolism; Edema - chemically induced; Edema - drug therapy; Edema - pathology; JAK/STATs; Janus Kinase Inhibitors - pharmacology; Janus Kinase Inhibitors - therapeutic use; Janus Kinases - antagonists & inhibitors; Lipopolysaccharides - pharmacology; Male; Mice; Mice, Inbred C57BL; Nitric Oxide - metabolism; Nitric Oxide Synthase Type II - genetics; Nitric Oxide Synthase Type II - metabolism; Oils, Volatile - pharmacology; Oils, Volatile - therapeutic use; RAW 264.7 Cells; Reactive Oxygen Species - metabolism; STAT Transcription Factors - antagonists & inhibitors; Tetradecanoylphorbol Acetate
• ISSN: 0378-8741; 1872-7573
• DOI: 10.1016/j.jep.2017.04.017

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. 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-κB/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. 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-α, IL-6, IFN-β 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-κB cascades. In animal model, oral administration of AAEO significantly attenuated TPA-induced mouse ear edema and decreased the protein level of COX-2. 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. [Display omitted]