View : 779 Download: 0
Cytotoxicity of lipid-soluble ginseng extracts is attenuated by plasma membrane redox enzyme NQO1 through maintaining redox homeostasis and delaying apoptosis in human neuroblastoma cells
- Title
- Cytotoxicity of lipid-soluble ginseng extracts is attenuated by plasma membrane redox enzyme NQO1 through maintaining redox homeostasis and delaying apoptosis in human neuroblastoma cells
- Authors
- Kim, Hwa-Kyung; Son, Tae Gen; Jo, Dong-Gyu; Kim, Dong Chung; Hyun, Dong-Hoon
- Ewha Authors
- 현동훈
- SCOPUS Author ID
- 현동훈
- Issue Date
- 2016
- Journal Title
- ARCHIVES OF PHARMACAL RESEARCH
- ISSN
- 0253-6269
1976-3786
- Citation
- ARCHIVES OF PHARMACAL RESEARCH vol. 39, no. 10, pp. 1339 - 1348
- Keywords
- Lipid-soluble ginseng extracts; NQO1; PMRS; Oxidative damage; Apoptosis
- Publisher
- PHARMACEUTICAL SOC KOREA
- Indexed
- SCIE; SCOPUS; KCI
- Document Type
- Review
- Abstract
- Lipid-soluble ginseng extracts (LSGE) is known to inhibit many types of cancer cells through arresting cell cycle and inducing apoptosis. Usually, normal cells are can also be damaged by anti-tumor reagents. The plasma membrane redox system (PMRS) is enhanced to compensate mitochondrial dysfunction and impaired energy metabolism. NADH-quinone oxidoreductase 1 (NQO1), a plasma membrane redox enzyme, is known to be induced by panaxytriol, one of components of lipid-soluble ginseng extracts (LSGE). The objective of this study was determine the mechanisms of NQO1 involved in neuroprotection in response to cytotoxicity induced by LSGE. Exposure of control SH-SY5Y cells to LSGE resulted in dramatic loss of cell viability in a dose-dependent manner. The loss of cell viability was significantly recovered in cells transfected with NQO1. LSGE-induced cell death occurred through apoptosis such as cell shrinkage, chromatin condensation and cleavage of poly (ADP-ribose) polymerase. These apoptotic features were significantly attenuated by overexpression of NQO1. Levels of oxidative/nitrative damage were highly elevated by LSGE in a dose-dependent manner. However, these elevated levels were greatly reduced by overexpression of NQO1. In addition, overexpression of NQO1 attenuated the decrease in mitochondrial complex I activity caused by LSGE. Taken together, these findings suggest that overexpressed NQO1 can protect cells against LSGE-induced cytotoxicity through lowering oxidative/nitrative damage and delaying apoptosis, supporting that stimulation of NQO1 activity could be a therapeutic targets in neurodegeration.
- DOI
- 10.1007/s12272-016-0817-6
- Appears in Collections:
- 자연과학대학 > 생명과학전공 > Journal papers
- Files in This Item:
There are no files associated with this item.
- Export
- RIS (EndNote)
- XLS (Excel)
- XML