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Transcriptional activation of Cu/Zn superoxide dismutase and catalase genes by panaxadiol ginsenosides extracted from Panax ginseng
Author(s) -
Chang Mun Seog,
Lee Seok Geun,
Rho Hyune Mo
Publication year - 1999
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/(sici)1099-1573(199912)13:8<641::aid-ptr527>3.0.co;2-z
Subject(s) - superoxide dismutase , catalase , ginseng , reactive oxygen species , biochemistry , antioxidant , sod1 , chemistry , enzyme , dismutase , microbiology and biotechnology , biology , medicine , alternative medicine , pathology
Superoxide dismutase (SOD) converts superoxide radical to H 2 O 2 , which is in turn broken down to water and oxygen by catalase. Thus, SOD and catalase constitute the first coordinated unit of defence against reactive oxygen species. A wide variety of chemical and environmental factors are known to induce these antioxidant enzymes. Here, we examined the effect of ginseng saponins on the induction of SOD and catalase gene expression. To explore this possibility, the upstream regulatory promoter region of Cu/Zn superoxide dismutase (SOD1) and catalase genes were linked to the chloramphenicol acetyltransferase (CAT) structural gene and introduced into human hepatoma HepG2 cells. Total saponin and panaxatriol did not activate the transcription of SOD1 and catalase genes but panaxadiol increased the transcription of these genes about 2–3 fold. Among the panaxadiol ginsenosides, the Rb 2 subfraction appeared to be a major inducer of SOD1 and catalase genes. The specificity of the Rb 2 effect was further confirmed by time course‐ and dose‐dependent induction experiments. These results suggest that the panaxadiol fraction and its ginsenosides could induce the antioxidant enzymes which are important for maintaining cell viability by lowering the level of oxygen radical generated from intracellular metabolism. Copyright © 1999 John Wiley & Sons, Ltd.