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http://dx.doi.org/10.5352/JLS.2013.23.6.736

Anti-inflammatory Effect of Achyranthoside E Dimethyl Ester in LPS-stimulated RAW 264.7 Cells  

Bang, Soo Young (Department of Molecular Biology, College of Natural Sciences, Pusan National University)
Kim, Ji-Hee (Department of Molecular Biology, College of Natural Sciences, Pusan National University)
Moon, Hyung-In (Department of Medicinal Biotechnology, College of Natural Resources and Life Science, Dong-A University)
Kim, Young Hee (Department of Molecular Biology, College of Natural Sciences, Pusan National University)
Publication Information
Journal of Life Science / v.23, no.6, 2013 , pp. 736-742 More about this Journal
Abstract
Achyranthoside E dimethyl ester (AEDE) is an oleanolic acid glycoside from Achyranthes japonica. In this study, we investigated the effects of AEDE on nitric oxide (NO) production and underlying molecular mechanisms in lipopolysaccharide (LPS)-stimulated macrophages. AEDE inhibited LPS-induced NO secretion as well as inducible NO synthase (iNOS) expression, without affecting cell viability. Further study demonstrated that AEDE induced heme oxygenase-1 (HO-1) gene expression. In addition, the inhibitory effects of AEDE on iNOS expression were abrogated by small interfering RNA-mediated knock-down of HO-1. Moreover, AEDE induced nuclear translocation of nuclear factor E2-related factor 2 (Nrf2), a transcription factor that regulates HO-1 expression. AEDE-induced expression of HO-1 was inhibited by inhibitors of phosphatidylinositol 3-kinase (PI-3K) and extracellular signal regulated kinase (ERK1/2). AEDE phosphorylated Akt and ERK1/2 as well. Therefore, these results suggest that AEDE suppresses the production of pro-inflammatory mediator such as NO by inducing HO-1 expression via PI-3K/Akt/ERK-Nrf2 signaling. These findings provide the scientific rationale for anti-inflammatory therapeutic use of AEDE.
Keywords
Achyranthoside E dimethyl ester; heme oxygenase-1; inducible nitric oxide synthase; NF-E2-related factor 2; nitric oxide;
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