Processed Panax ginseng, Sun Ginseng, Decreases Oxidative Damage Induced by tert-butyl Hydroperoxide via Regulation of Antioxidant Enzyme and Anti-apoptotic Molecules in HepG2 CellsProcessed Panax ginseng, Sun Ginseng, Decreases Oxidative Damage Induced by tert-butyl Hydroperoxide via Regulation of Antioxidant Enzyme and Anti-apoptotic Molecules in HepG2 Cells
- Other Titles
- 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
- 이혜진; Jinhee Kim; 이서영; 박정일; 황귀서
- Issue Date
- Jul-2012
- Publisher
- 고려인삼학회
- Keywords
- Panax ginseng; Sun ginseng; Antioxidant activity; tert-butyl hydroperoxide; HepG2
- Citation
- Journal of Ginseng Research, v.36, no.3, pp 248 - 255
- Pages
- 8
- Journal Title
- Journal of Ginseng Research
- Volume
- 36
- Number
- 3
- Start Page
- 248
- End Page
- 255
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/61987
- DOI
- 10.5142/jgr.2012.36.3.248
- ISSN
- 1226-8453
2093-4947
- 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 signifi cant change in SG-treated HepG2 cells. These fi ndings 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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