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      Ginsenoside Rc from Panax ginseng exerts anti-inflammatory activity by targeting TANK-binding kinase 1/interferon regulatory factor-3 and p38/ATF-2

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          Abstract

          Background

          Ginsenoside Rc (G-Rc) is one of the major protopanaxadiol-type saponins isolated from Panax ginseng, a well-known medicinal herb with many beneficial properties including anticancer, anti-inflammatory, antiobesity, and antidiabetic effects. In this study, we investigated the effects of G-Rc on inflammatory responses in vitro and examined the mechanisms of these effects.

          Methods

          The in vitro inflammation system used lipopolysaccharide-treated macrophages, tumor necrosis factor-α/interferon-γ-treated synovial cells, and HEK293 cells transfected with various inducers of inflammation.

          Results

          G-Rc significantly inhibited the expression of macrophage-derived cytokines, such as tumor necrosis factor-α and interleukin-1β. G-Rc also markedly suppressed the activation of TANK-binding kinase 1/IκB kinase ε/interferon regulatory factor-3 and p38/ATF-2 signaling in activated RAW264.7 macrophages, human synovial cells, and HEK293 cells.

          Conclusion

          G-Rc exerts its anti-inflammatory actions by suppressing TANK-binding kinase 1/IκB kinase ε/interferon regulatory factor-3 and p38/ATF-2 signaling.

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          Most cited references25

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          Cardiovascular Diseases and Panax ginseng: A Review on Molecular Mechanisms and Medical Applications

          Jong-Hoon Kim (2012)
          Ginseng is one of the most widely used herbal medicines and is reported to have a wide range of therapeutic and pharmacological applications. Ginseng may also be potentially valuable in treating cardiovascular diseases. Research concerning cardiovascular disease is focusing on purified individual ginsenoside constituents of ginseng to reveal specific mechanisms instead of using whole ginseng extracts. The most commonly studied ginsenosides are Rb1, Rg1, Rg3, Rh1, Re, and Rd. The molecular mechanisms and medical applications of ginsenosides in the treatment of cardiovascular disease have attracted much attention and been the subject of numerous publications. Here, we review the current literature on the myriad pharmacological functions and the potential benefits of ginseng in this area. In vitro investigations using cell cultures and in vivo animal models have indicated ginseng’s potential cardiovascular benefits through diverse mechanisms that include antioxidation, modifying vasomotor function, reducing platelet adhesion, influencing ion channels, altering autonomic neurotransmitters release, and improving lipid profiles. Some 40 ginsenosides have been identified. Each may have different effects in pharmacology and mechanisms due to their different chemical structures. This review also summarizes results of relevant clinical trials regarding the cardiovascular effects of ginseng, particularly in the management of hypertension and improving cardiovascular function.
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            Functional Roles of Syk in Macrophage-Mediated Inflammatory Responses

            Young-Su Yi, Young-Jin Son, Chongsuk Ryou … (2014)
            Inflammation is a series of complex biological responses to protect the host from pathogen invasion. Chronic inflammation is considered a major cause of diseases, such as various types of inflammatory/autoimmune diseases and cancers. Spleen tyrosine kinase (Syk) was initially found to be highly expressed in hematopoietic cells and has been known to play crucial roles in adaptive immune responses. However, recent studies have reported that Syk is also involved in other biological functions, especially in innate immune responses. Although Syk has been extensively studied in adaptive immune responses, numerous studies have recently presented evidence that Syk has critical functions in macrophage-mediated inflammatory responses and is closely related to innate immune response. This review describes the characteristics of Syk-mediated signaling pathways, summarizes the recent findings supporting the crucial roles of Syk in macrophage-mediated inflammatory responses and diseases, and discusses Syk-targeted drug development for the therapy of inflammatory diseases.
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              Role of vascular smooth muscle cell in the inflammation of atherosclerosis

              Soyeon Lim, Sungha Park (2014)
              Atherosclerosis is a pathologic process occurring within the artery, in which many cell types, including T cell, macrophages, endothelial cells, and smooth muscle cells, interact, and cause chronic inflammation, in response to various inner- or outer-cellular stimuli. Atherosclerosis is characterized by a complex interaction of inflammation, lipid deposition, vascular smooth muscle cell proliferation, endothelial dysfunction, and extracellular matrix remodeling, which will result in the formation of an intimal plaque. Although the regulation and function of vascular smooth muscle cells are important in the progression of atherosclerosis, the roles of smooth muscle cells in regulating vascular inflammation are rarely focused upon, compared to those of endothelial cells or inflammatory cells. Therefore, in this review, we will discuss here how smooth muscle cells contribute or regulate the inflammatory reaction in the progression of atherosclerosis, especially in the context of the activation of various membrane receptors, and how they may regulate vascular inflammation. [BMB Reports 2014; 47(1): 1-7]
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                Author and article information

                Contributors
                Tao Yu
                Man Hee Rhee
                Jae Youl Cho
                Journal
                Journal ID (nlm-ta): J Ginseng Res
                Journal ID (iso-abbrev): J Ginseng Res
                Title: Journal of Ginseng Research
                Publisher: Elsevier
                ISSN (Print): 1226-8453
                ISSN (Electronic): 2093-4947
                Publication date PMC-release: 10 February 2016
                Publication date (Print): April 2017
                Publication date (Electronic): 10 February 2016
                Volume: 41
                Issue: 2
                Pages: 127-133
                Affiliations
                [1 ]Department of Genetic Engineering, Sungkyunkwan University, Suwon, Korea
                [2 ]Institute of Translational Medicine, Qingdao University, Qingdao, China
                [3 ]Korean Ginseng Corporation, Central Research Institute, Daejeon, Korea
                [4 ]Division of Rheumatology, Department of Internal Medicine, Korea University Guro Hospital, Seoul, Korea
                [5 ]Department of Bioinformatics and Life Science, Soongsil University, Seoul, Korea
                [6 ]College of Veterinary Medicine, Kyungpook National University, Daegu, Korea
                Author notes
                [∗ ]Corresponding author. Department of Genetic Engineering, Sungkyunkwan University, 300 Chuncheon-Dong, Suwon 16419, Korea. jaecho@ 123456skku.edu
                [∗∗ ]Corresponding author. Institute of Translational Medicine, Qingdao University, 38 Dengzhou, Qingdao 266071, China. yutao0112@ 123456qdu.edu.cn
                [∗∗∗ ]Corresponding author. College of Veterinary Medicine, Kyungpook National University, 80 Daehakro, Bukgu, Daegu 41566, Korea. rheemh@ 123456knu.ac.kr
                Article
                Publisher ID: S1226-8453(16)00007-5
                DOI: 10.1016/j.jgr.2016.02.001
                PMC ID: 5386129
                PubMed ID: 28413316
                SO-VID: 8ef7a755-7791-4963-abb1-431694d1d615
                Copyright © © 2017 The Korean Society of Ginseng, Published by Elsevier Korea LLC.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 19 January 2016
                Date revision received : 30 January 2016
                Date accepted : 2 February 2016
                Categories
                Subject: Research Article

                Keywords: anti-inflammatory activity,ginsenoside rc,p38,panax ginseng,tank-binding kinase 1
                Data availability:
                Keywords: anti-inflammatory activity, ginsenoside rc, p38, panax ginseng, tank-binding kinase 1

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