Anti-Inflammatory Effect of Rhapontici Radix Ethanol Extract via Inhibition of NF-κB and MAPK and Induction of HO-1 in Macrophages.

Yun Hee Jeong,You-Chang Oh,Nam-Hui Yim,Won-Kyung Cho,Jin Yeul Ma

doi:10.1155/2016/7216912

Yun Hee Jeong, You-Chang Oh + Show 3 more

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https://doi.org/10.1155/2016/7216912

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Abstract

Rhapontici Radix (RR) has been used in traditional medicine in East Asia and has been shown to have various beneficial effects. However, its biological properties or mechanism on inflammation-related diseases is unknown. The goal of this study was to determine the anti-inflammatory activity and underlying molecular mechanisms of Rhapontici Radix ethanol extract (RRE). The inhibitory effect of RRE on the production of NO, cytokines, inflammatory-related proteins, and mRNAs in LPS-stimulated macrophages was determined by the Griess assay, ELISA, Western blot analysis, and real-time RT-PCR, respectively. Our results indicate that treatment with RRE significantly inhibited the secretion of NO and inflammatory cytokines in RAW 264.7 cells and mouse peritoneal macrophages without cytotoxicity. We also found that RRE strongly suppressed the expression of iNOS and COX-2 and induced HO-1 expression. It also prevented nuclear translocation of NF-κB by inhibiting the phosphorylation and degradation of IκBα. Furthermore, the phosphorylation of MAPKs in LPS-stimulated RAW 264.7 cells was significantly inhibited by RRE. These findings suggest that RRE may operate as an effective anti-inflammatory agent by inhibiting the activation of NF-κB and MAPK signaling pathways and inducing HO-1 expression in macrophages. Our results suggest that RRE has potential value as candidate to inflammatory therapeutic phytomedicine.

Highlights

Inflammation is a highly regulated defensive process that results from tissue injury or infection
The viability of the cells treated with Rhapontici Radix ethanol extract (RRE) is shown in Figure 1(a), which indicates that a concentration of up to 100 μg/mL RRE was associated with no significant change in overall cell viability
We found that RRE dramatically inhibited the release of nitric oxide (NO) in a dosedependent manner upon LPS stimulation (Figure 1(b))

Summary

Introduction

Inflammation is a highly regulated defensive process that results from tissue injury or infection. Lipopolysaccharide (LPS) treatment of the murine macrophage cell line RAW 264.7 results in the production of many inflammatory mediators, such as nitric oxide (NO), inducible nitric oxide synthase (iNOS), cyclooxygenase- (COX-) 2, tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, and IL-1β [2,3,4]. The expression of these factors is induced by the activation of nuclear factor- (NF-) κB and mitogen-activated protein kinases (MAPKs) in macrophages [5,6,7]. A number of previous studies have shown that various naturally derived substances exert antiinflammatory effects by inhibiting the NF-κB and MAPK signaling pathways [8,9,10]

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