Artemisinin inhibits inflammatory response via regulating NF-kappa B and MAPK signaling pathways

作者：Wang, Ke Si; Li, Junbo; Wang, Zhe; Mi, Chunliu; Ma, Juan; Piao, Lian Xun; Xu, Guang Hua; Li, Xuezheng; Jin, Xuejun^*

来源：Immunopharmacology and Immunotoxicology, 2017, 39(1): 28-36.

DOI：10.1080/08923973.2016.1267744

• Artemisinin
• Inflammation
• I kappa B alpha
• MAPK
• Nuclear factor-kappa B (NF-kappa B)

Artemisinin, isolated from the Chinese plant Artemisia annua, has been used for many years to treat different forms of malarial parasites. In this study, we explored the anti-inflammatory activity of artemisinin and the underlying mechanism of this action. We demonstrated that the anti-inflammatory effects of artemisinin in TPA-induced skin inflammation in mice. Then the artemisinin significantly inhibited the expression of NF-kappa B reporter gene induced by TNF-alpha in a dose-dependent manner. Artemisinin also inhibited TNF-alpha induced phosphorylation and degradation of I kappa B alpha, p65 nuclear translocation. Artemisinin also has an impact on upstream signaling of IKK through the inhibition of expression of adaptor proteins, TNF receptor-associated factor 2 (TRAF2) and receptor interacting protein 1 (RIP1). Furthermore, pretreatment of cells with artemisinin prevented the TNF-alpha-induced expression of NF-kappa B target genes, such as anti-apoptosis (c-IAP1, Bcl-2, and FLIP), proliferation (COX-2, cyclinD1), invasion (MMP-9), angiogenesis (VEGF), and major inflammatory cytokines (TNF-alpha, iNOS, and MCP1). We also proved that artemisinin potentiated TNF-alpha-induced apoptosis. Moreover, artemisinin significantly impaired the ROS production and phosphorylation of p38 and ERK, but did not affect the phosphorylation of JNK. Taken together, artemisinin may be a potentially useful therapeutic agent for inflammatory-related diseases.

• 出版日期2017-2
• 单位延边大学