The Effects of Ginsenoside Rb1 on the Apoptosis and the Production of Nitric Oxide in Rat C6 Glioma Cells.
- Author:
Joo Hyeon PARK
1
;
Yoon Hee LEE
;
Ku Seong KANG
;
Soo Kyoung LEE
;
Sun Zoo KIM
;
Ji Young PARK
;
Eun Kyoung KWAK
;
Yoon Kyung SOHN
Author Information
1. Department of Pathology, School of Medicine, Kyungpook National University, Daegu, Korea. yksohn@knu.ac.kr
- Publication Type:Original Article
- Keywords:
Cultured Tumor Cells;
Ginsenoside;
Apoptosis;
Nitric Oxide Synthase;
Nitric Oxide
- MeSH:
Animals;
Apoptosis*;
Ginsenosides;
Glioma*;
Interferons;
Nitric Oxide Synthase;
Nitric Oxide*;
Panax;
Rats*;
RNA, Messenger;
Tumor Cells, Cultured;
Tumor Necrosis Factor-alpha
- From:Korean Journal of Pathology
2004;38(1):1-7
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Ginsenosides, the extract of Panax ginseng, exert various pharmacological effects such as anticancer activity by the mechanism that is not yet defined. In this study, we proposed that the anticancer effect of ginsenoside Rb1 is related to tumor cell apoptosis and ginsenoside Rb1 induces the tumor cell apoptosis via the nitric oxide (NO) production. METHODS: Rat C6 glioma cells were activated by treating with lipopolysaccharide (LPS), interferon (IFN)-gamma , and tumor necrosis factor (TNF)-alpha on the culture medium to investigate the effects of ginsenoside Rb1. RESULTS: Compared with C6 glioma cells treated with LPS/IFN-gamma/TNF-alpha, C6 glioma cells treated with LPS/IFN-gamma/TNF-alpha/ginsenoside Rb1 showed marked increase in the NO production and apoptosis. Ginsenoside Rb1 induces the NO production in C6 glioma cells in dose-dependent manner. When C6 glioma cells treated with LPS/IFN-gamma/TNF-alpha/ginsenoside Rb1 were incubated with the specific inhibitor of iNOS, S-Methyl-2-thiopseudoureasulfate (SMT), both NO production and apoptosis in C6 glioma cells was significantly decreased. Ginsenoside Rb1 induced the expression of iNOS mRNA and iNOS protein in C6 glioma cells. CONCLUSIONS: These results suggest that the induction of iNOS expression and subsequent
