scholarly journals Effects of Korean Red Ginseng (Panax ginseng C.A. Mayer) and Its Isolated Ginsenosides and Polysaccharides on Arterial Stiffness in Healthy Individuals

2010 ◽  
Vol 23 (5) ◽  
pp. 469-472 ◽  
Author(s):  
E. Jovanovski ◽  
A. Jenkins ◽  
A. G. Dias ◽  
V. Peeva ◽  
J. Sievenpiper ◽  
...  
2011 ◽  
Vol 137 (1) ◽  
pp. 245-250 ◽  
Author(s):  
Leanne R. De Souza ◽  
Alexandra L. Jenkins ◽  
John L. Sievenpiper ◽  
Elena Jovanovski ◽  
Dario Rahelić ◽  
...  

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Jyoti Bhardwaj ◽  
Emma Bateman ◽  
Clarissa Sam ◽  
Elena Jovanovski ◽  
Christopher Fairgrieve ◽  
...  

2012 ◽  
Vol 144 (2) ◽  
pp. 225-233 ◽  
Author(s):  
Young Joo Hong ◽  
Nayoung Kim ◽  
Karim Lee ◽  
Chung Hee Sonn ◽  
Jung Eun Lee ◽  
...  

2016 ◽  
Vol 44 (03) ◽  
pp. 595-615 ◽  
Author(s):  
Tao Yu ◽  
Man Hee Rhee ◽  
Jongsung Lee ◽  
Seung Hyung Kim ◽  
Yanyan Yang ◽  
...  

Korean Red Ginseng (KRG) is an herbal medicine prescribed worldwide that is prepared from Panax ginseng C.A. Meyer (Araliaceae). Out of ginseng’s various components, ginsenosides are regarded as the major ingredients, exhibiting anticancer and anti-inflammatory activities. Although recent studies have focused on understanding the anti-inflammatory activities of KRG, compounds that are major anti-inflammatory components, precisely how these can suppress various inflammatory processes has not been fully elucidated yet. In this study, we aimed to identify inhibitory saponins, to evaluate the in vivo efficacy of the saponins, and to understand the inhibitory mechanisms. To do this, we employed in vitro lipopolysaccharide-treated macrophages and in vivo inflammatory mouse conditions, such as collagen (type II)-induced arthritis (CIA), EtOH/HCl-induced gastritis, and lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-triggered hepatitis. Molecular mechanisms were also verified by real-time PCR, immunoblotting analysis, and reporter gene assays. Out of all the ginsenosides, ginsenoside Rc (G-Rc) showed the highest inhibitory activity against the expression of tumor necrosis factor (TNF)-[Formula: see text], interleukin (IL)-1[Formula: see text], and interferons (IFNs). Similarly, this compound attenuated inflammatory symptoms in CIA, EtOH/HCl-mediated gastritis, and LPS/D-galactosamine (D-GalN)-triggered hepatitis without altering toxicological parameters, and without inducing gastric irritation. These anti-inflammatory effects were accompanied by the suppression of TNF-[Formula: see text] and IL-6 production and the induction of anti-inflammatory cytokine IL-10 in mice with CIA. G-Rc also attenuated the increased levels of luciferase activity by IRF-3 and AP-1 but not NF-[Formula: see text]B. In support of this phenomenon, G-Rc reduced TBK1, IRF-3, and ATF2 phosphorylation in the joint and liver tissues of mice with hepatitis. Therefore, our results strongly suggest that G-Rc may be a major component of KRG with useful anti-inflammatory properties due to its suppression of IRF-3 and AP-1 pathways.


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