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Processed Panax ginseng, Sun Ginseng, Decreases Oxidative Damage Induced by tert-butyl Hydroperoxide via Regulation of Antioxidant Enzyme and Anti-apoptotic Molecules in HepG2 Cells

Authors
Lee, HyejinKim, JinheeLee, Seo YoungPark, Jeong HillHwang, Gwi Seo
Issue Date
Jul-2012
Publisher
KOREAN SOC GINSENG
Keywords
Panax ginseng; Sun ginseng; Antioxidant activity; tert-butyl hydroperoxide; HepG2
Citation
JOURNAL OF GINSENG RESEARCH, v.36, no.3, pp.248 - 255
Journal Title
JOURNAL OF GINSENG RESEARCH
Volume
36
Number
3
Start Page
248
End Page
255
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/16297
DOI
10.5142/jgr.2012.36.3.248
ISSN
1226-8453
Abstract
Potential antioxidant effect of processed ginseng (sun ginseng, SG) on oxidative stress generated by tert-butyl hydroperoxide (t-BHP) was investigated in HepG2 cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and lactate dehydrogenase (LDH) leakage test demonstrated that SG dose-dependently prevents a loss of cell viability against t-BHP-induced oxidative stress. Also, SG treatment dose-dependently relieved the increment of activities of hepatic enzymes, such as aspartate aminotrasferase and alanine aminotransferase, and lipid peroxidation mediated by t-BHP treatment in HepG2 cells. SG increased the gene expression of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. However, high dose of SG treatment caused decrease in mRNA level of glutathione peroxidase as compared to low dosage of SG-treated cells. The gene expression of glutathione reductase was found to be slightly increased by SG treatment. In addition, SG extract attributed its hepaprotective effect by inducing the mRNA level of bcl-2 and bcl-xL, but reducing that of bax. But, the gene expression of bad showed no significant change in SG-treated HepG2 cells. These findings suggest that SG has hepatoprotective effect by showing reduction of LDH release, activities of hepatic enzymes and lipid peroxidation and regulating the gene expression of antioxidant enzymes and apoptosis-related molecules against oxdative stress caused by t-BHP in HepG2 cells.
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