Anti-inflammatory potential of Phaseolus calcaratus Roxburgh, a oriental medicine, on LPS-stimulated RAW 264.7 macrophages |
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Authors: | Fang Minghao Lee Seung-Youp Park Seung-Moon Choi Ki-Choon Lee Young Jae Cho Hyoung-Kwon Cho Seong-Wan Whang Wan Kyunn Lee Jeong-Chae |
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Affiliation: | Department of Orthodontics and Institute of Oral Biosciences, BK21 program and School of Dentistry, Chonbuk National University, Jeonju, Republic of Korea. |
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Abstract: | Objectives The seed of Phaseolus calcaratus Roxburgh (PHCR) has traditionally been used as a herbal medicine, considered to have anti‐inflammatory potential. Here we examined the ability of PHCR seed extract to inhibit inflammatory responses of macrophages to bacterial toxin and the mechanism involved. Methods In the present study, we prepared four fractions from an ethanol extract of PHCR seed and investigated their effects on the production of nitric oxide and cytokines, and the expression of inducible nitric oxide synthase (iNOS) in lipopolysaccharide (LPS)‐stimulated RAW 264.7 macrophage cells. Key findings The fractions inhibited LPS‐induced nitric oxide production and cyclooxygenase‐2 (COX‐2) expression in the cells. The ethyl acetate fraction at 100 µg/ml almost completely suppressed NO production, iNOS and COX‐2 expression, and TNF‐α and IL‐6 secretion in cells stimulated with LPS. The fraction also inhibited phosphorylation of extracellular signal‐regulated kinase (ERK) and p38 in LPS‐stimulated cells with the attendant suppression of IκBα nuclear translocation and nuclear factor (NF)‐κB activation. Furthermore, PHCR seed extracts contained a large number of phenolic compounds having antioxidant potentials against 1,1‐diphenyl‐2‐picrylhydrazyl (DPPH) radicals and hydroxyl radicals. We identified catechin‐7‐O‐β‐d ‐glucopyranoside as one of the active compounds responsible for the biological activity of PHCR seed extract. Conclusions These results suggest for the first time that ethanol extracts from PHCR seed have anti‐inflammatory potential on LPS‐stimulated macrophages through the down‐regulation of ERK/p38‐ and NF‐κB‐mediated signalling pathways. |
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Keywords: | anti‐inflammation lipopolysaccharide mitogen‐activated protein kinase nuclear factor‐κB Phaseolus calcaratus R |
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