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Anti‐inflammatory Effects of Ginsenosides Rg 5 , Rz 1 , and Rk 1 : Inhibition of TNF‐α‐induced NF‐κB, COX‐2, and iNOS transcriptional expression
Author(s) -
Lee Sang Myung
Publication year - 2014
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.5203
Subject(s) - chemistry , nf κb , pharmacology , tumor necrosis factor alpha , ginsenoside , luciferase , nfkb1 , ginseng , sulfasalazine , gene expression , anti inflammatory , apoptosis , biochemistry , biology , immunology , medicine , gene , transfection , pathology , transcription factor , alternative medicine , disease , ulcerative colitis
In the course of this experiment on the anti‐inflammatory effect of ginsenosides, protopanaxdiol ginsenosides have shown inhibition activities in inflammatory responses: NF‐κB, COX‐2, and iNOS were induced by TNF‐α. The responses of this experiment were evaluated by NF‐κB‐luciferase assay and RT‐PCR experiment of COX‐2 and iNOS genes. The NF‐κB expressions were inhibited by ginsenosides Rd, Rg 5 , Rz 1 , and Rk 1 in a dose‐dependent manner. The IC 50 values were 3.47, 0.61, 0.63, and 0.75 μM, respectively. Particularly, ginsenosides Rg 5 , Rz 1 , and Rk 1 as converted ginsenosides from primary protopanaxdiol ginsenosidess significantly inhibited COX‐2 and iNOS gene expression. These inhibition levels were similar to sulfasalazine as reference material. Copyright © 2014 John Wiley & Sons, Ltd.