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Year : 2014  |  Volume : 10  |  Issue : 39  |  Page : 588-595

Anti-inflammatory effect of Artemisiae annuae herba in lipopolysaccharide-stimulated RAW 264.7 Cells

Korean Medicine-Based Herbal Drug Development Group, Korea Institute of Oriental Medicine, Daejeon 305-811, South Korea

Correspondence Address:
Jin Yeul Ma
461-24, Jeonmin dong, Yuseong, Daejeon 305-811
South Korea
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Source of Support: This work was supported by the grant (K14050) from the Korea Institute of Oriental Medicine funded by the Ministry of Education, Science and Technology (MEST), the Republic of Korea., Conflict of Interest: None

DOI: 10.4103/0973-1296.139793

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Background: Artemisiae annuae herba (AAH) has been traditionally used as a drug for the treatment of malaria, heat stroke, bacterial infection, and fever in East-Asia. Although AAH has been used for the treatment of inflammation-related symptoms, the underlying mechanism of antiinflammatory activity of AAH is still unknown. Objective: We investigated whether AAH have an inhibitory effect on the production of pro-inflammatory mediators in lipopolysaccharide-stimulated RAW 264.7 macrophage cells. Materials and Methods: The investigation was forced on the inhibitory effect of AAH on the production of tumor necrosis factor (TNF)-α, interleukin (IL)-6, nitric oxide (NO), and inducible NO synthase (iNOS) in macrophages. Furthermore, we examined the effect of AAH on the activation of nuclear factor kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs) pathways. Results: We found that AAH suppresses NO production and TNF-α, IL-6, and iNOS gene expression. Moreover, AAH inhibited the nuclear translocation of p65 and IκBα degradation in NF-κB pathway and decreased the extracellular signal-regulated kinase, p38, c-Jun NH 2 -terminal kinase phosphorylation in MAPK signaling pathway. Conclusions: Consequently, these results indicate that AAH contains antiinflammatory activity and this effect is derived from the repression on the activation of NF-κB and MAPKs pathways. We first demonstrated that antiinflammatory effect of AAH and its underlying mechanism in macrophage cells.

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