The Antiinflammatory Mechanism of Igongsan in Mouse Peritoneal Macrophages via Suppression of NF‐κB/Caspase‐1 Activation |
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Authors: | Dae‐Seung Kim Jong Hyun Lee Mi‐Young Jeong Hye‐Lin Kim Jinbong Park Hara Lim Sung‐Hoon Kim Seung‐Heon Hong Min‐Woo Hwang Jae‐Young Um |
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Affiliation: | 1. College of Pharmacy, Wonkwang University, , Iksan, Jeonbuk, 570‐749 Korea;2. College of Pharmacy, Dongduk Women's University, , Seongbuk‐gu, Seoul, Korea;3. College of Korean Medicine, Institute of Korean Medicine, Kyung Hee University, , Dongdaemun‐Gu, Seoul, 130‐701 Korea |
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Abstract: | Igongsan (IGS), which is an herbal prescription composed of five different herbs, Ginseng Radix (root of Panax ginseng, Araliaceae), Atractylodis Rhizoma Alba (rhizome of Atractylodes Macrocephala, Compositae), Poria Sclerotium (sclerotium of Poria cocos, Polyporaceae), Glycyrrhizae Radix et Rhizoma (root and rhizome of Glycyrrhiza uralensis, Leguminosae), and Citri Unshius Pericarpium (Peel of Citrus unshiu, Rutaceae), has been traditionally used in Korea to treat a variety of inflammatory diseases. In this study, we investigated to elucidate the mechanism responsible for IGS's antiinflammatory effect in mouse peritoneal macrophages. The findings demonstrate that IGS inhibited the production of inflammatory cytokine and prostaglandins E2. IGS inhibited the enhanced levels of cyclooxygenase‐2 and inducible NO synthase caused by lipopolysaccharide (LPS). Additionally, it was shown that the antiinflammatory effect of IGS is through regulating the activation of nuclear factor‐kappa B and caspase‐1 in LPS‐stimulated mouse peritoneal macrophages. These results provide novel insights into the pharmacological actions of IGS as a potential candidate for development of new drugs to treat inflammatory diseases. Discussion and conclusion: These results provide novel insights into the pharmacological actions of IGS as a potential candidate for development of new drugs to treat inflammatory diseases. Copyright © 2013 John Wiley & Sons, Ltd. |
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Keywords: | igongsan inflammation macrophage nuclear factor‐kappa B caspase‐1 |
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