Role of ginsenosides, the main active components of Panax ginseng, in inflammatory responses and diseases

Posted by Michael Burmeister on

Ji Hye Kim,1, Young-Su Yi,2, Mi-Yeon Kim,3, and Jae Youl Cho1


Panax ginseng is one of the most universally used herbal medicines in Asian and Western countries. Most of the biological activities of ginseng are derived from its main constituents, ginsenosides. Interestingly, a number of studies have reported that ginsenosides and their metabolites/derivatives—including ginsenoside (G)-Rb1, compound K, G-Rb2, G-Rd, G-Re, G-Rg1, G-Rg3, G-Rg5, G-Rh1, G-Rh2, and G-Rp1—exert anti-inflammatory activities in inflammatory responses by suppressing the production of proinflammatory cytokines and regulating the activities of inflammatory signaling pathways, such as nuclear factor-κB and activator protein-1. This review discusses recent studies regarding molecular mechanisms by which ginsenosides play critical roles in inflammatory responses and diseases, and provides evidence showing their potential to prevent and treat inflammatory diseases.

Keywords: ginsenosides, inflammation, inflammatory diseases, Panax ginseng, signaling

1. Introduction

The immune response is the most important defense system protecting the human body from external attacks by microorganisms and toxic chemical compounds. In order for this function to work properly, it is necessary to distinguish pathogens from the body's own cells or tissues. However, pathogens can avoid the immune system through various mechanisms. Therefore, multiple approaches that recognize and neutralize pathogens have been developed to overcome these difficulties. The immune system uses a layered defense strategy against infection based on gradually increasing specificity for invading organisms . Innate immunity is the first line of defense, composed of four kinds of barriers: physical, physiological, phagocytosis, and inflammation (Table 1). Innate immunity acts mainly to detect invading microorganisms by recognizing their pathogen-associated molecular patterns , and therefore acts in a comprehensive manner against pathogens. In addition, the immune response is not long-lasting . Adaptive immunity, also known as acquired immunity, is the second line of defense and has two important processes that are distinguished from those of innate immunity: presenting antigens and developing immunological memory (Table 2) . Adaptive immunity is divided into two types of immune responses: humoral immune response and cell-mediated immune response . The humoral immune response is mediated by antibodies produced by B cells in body fluids, which collaborate with complements secreted by hepatocytes or macrophages , . The cell-mediated immune response refers to the process in which immune cells detect and destroy nonself cells , and consists of two responses. Of the two, the antigen-specific reaction is caused by cytotoxic T cells that are produced to destroy antigen-displaying cells by recognizing major histocompatibility complex class I molecule- and endogenous antigen-presenting cells, whereas nonspecific reactions take place when major histocompatibility complex class II molecules and exogenous antigens are presented on the cell membrane. In this response, helper T cells are produced and secrete interleukins and cytokines to stimulate B cells . In turn, the stimulated B cells produce antigen-specific antibodies and activate natural killer cells and macrophages to eliminate the infected cells .


Studies of the pharmacological roles of ginsenosides have focused mostly on their anticancer, antioxidative, and immunostimulatory activities. A number of recent studies, however, have presented evidence showing that ginsenosides could be used to prevent and treat a variety of inflammatory diseases via anti-inflammatory functions (Table 4). In particular, considering the action mechanisms of ginsenosides, they are expected to regulate inflammatory responses primarily through the inhibition of the NF-κB signaling pathway. In LPS-stimulated macrophages and microglial cells, ginsenosides suppress the production of proinflammatory cytokinases such as TNF-α, IL-1β, and IL-6, as well as inflammatory enzymes, such as iNOS and COX-2. The expression of these molecules is predominantly regulated by NF-κB signaling pathways, where IRAK, IKKα/β, and IκBα are included in inflammatory responses. According to the results of many in vitro studies, ginsenosides exert anti-inflammatory activities in a variety of in vivo animal models of inflammatory diseases, and show promising protective effects in animal models of colitis, alcohol-induced hepatitis, IR injury, and impaired memory diseases. Furthermore, the biological activities of ginsenoside metabolites, such as CK, G-Rh1, and G-Rh2, have been observed in diverse inflammation models. CK is effective for ameliorating symptoms in animal models of ear edema, colitis, and lethal shock. G-Rh1 and G-Rh1 also exerted anti-inflammatory effects in animal models of atopic dermatitis and asthma.

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