Effects of Panax ginseng on Tumor Necrosis Factor-α-Mediated Inflammation: A Mini-Review

被引:87
作者
Lee, Davy C. W. [1 ]
Lau, Allan S. Y. [1 ,2 ]
机构
[1] Univ Hong Kong, Cytokine Biol Grp, Dept Paediat & Adolescent Med, Pokfulam, Hong Kong, Peoples R China
[2] Univ Hong Kong, Mol Chinese Med Lab, Li Ka Shing Fac Med, Pokfulam, Hong Kong, Peoples R China
关键词
Panax ginseng; ginsenosides; cytokines; immunomodulation; inflammation; NF-KAPPA-B; COLLAGEN-INDUCED ARTHRITIS; NITRIC-OXIDE SYNTHASE; KINASE-A PATHWAY; TNF-ALPHA; ANTIINFLAMMATORY MECHANISM; IMMUNOMODULATOR GINSAN; ACIDIC POLYSACCHARIDES; STIMULATED MICROGLIA; NOTOGINSENG SAPONINS;
D O I
10.3390/molecules16042802
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Panax ginseng is one of the most commonly used Chinese medicines in China, Asia and Western countries. The beneficial effects of ginseng have been attributed to the biological activities of its constituents, the ginsenosides. In this review, we summarize recent publications on the anti-inflammatory effects of ginseng extracts and ginsenosides on cellular responses triggered by different inducers including endotoxin, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma and other stimuli. Proinflammatory cytokines, chemokines, adhesion molecules and mediators of inflammation including inducible nitric oxide synthase, cyclooxygenase-2 and nitric oxide orchestrate the inflammatory response. Ginseng extracts and ginsenosides including Rb-1, Rd, Rg(1), Rg(3), Rh-1, Rh-2, Rh-3 and Rp(1) have been reported to have anti-inflammatory properties in different studies related to inflammation. Ginsenosides inhibit different inducers-activated signaling protein kinases and transcription factor nuclear factor-kappaB leading to decreases in the production of cytokines and mediators of inflammation. The therapeutic potential of ginseng on TNF-alpha-mediated inflammatory diseases is also discussed. Taken together, this summary provides evidences for the anti-inflammatory effects of ginseng extracts and ginsenosides as well as the underlying mechanisms of their effects on inflammatory diseases.
引用
收藏
页码:2802 / 2816
页数:15
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