Comparison of anticancer activities of Korean Red Ginseng-derived fractions

被引:25
作者
Baek, Kwang-Soo [1 ]
Yi, Young-Su [2 ]
Son, Young-Jin [3 ]
Jeong, Deok [1 ]
Sung, Nak Yoon [1 ]
Aravinthan, Adithan [4 ]
Kim, Jong-Hoon [4 ]
Cho, Jae Youl [1 ]
机构
[1] Sungkyunkwan Univ, Dept Genet Engn, 2066 Seobu Ro, Suwon 16419, South Korea
[2] Cheongju Univ, Dept Pharmaceut Engn, Cheongju, South Korea
[3] Sunchon Natl Univ, Dept Pharm, Sunchon, South Korea
[4] Chonbuk Natl Univ, Dept Physiol, Coll Vet Med, 79 Gobong Ro, Iksan 54596, South Korea
关键词
antitumorigenic activity; Korean Red Ginseng; nonsaponin fraction; saponin fraction; xenograft mouse model; MOLECULAR-MECHANISMS; HERBAL MEDICINES; CANCER; ACTIVATION; EXTRACT; CELLS;
D O I
10.1016/j.jgr.2016.11.001
中图分类号
Q94 [植物学];
学科分类号
071001 [植物学];
摘要
Background: Korean Red Ginseng (KRG) is an ethnopharmacological plant that is traditionally used to improve the body's immune functions and ameliorate the symptoms of various diseases. However, the antitumorigenic effects of KRG and its underlying molecular and cellular mechanisms are not fully understood in terms of its individual components. In this study, in vitro and in vivo antitumorigenic activities of KRG were explored in water extract (WE), saponin fraction (SF), and nonsaponin fraction (NSF). Methods: In vitro antitumorigenic activities of WE, SF, and NSF of KRG were investigated in the C6 glioma cell line using cytotoxicity, migration, and proliferation assays. The underlying molecular mechanisms of KRG fractions were determined by examining the signaling cascades of apoptotic cell death by semiquantitative reverse transcriptase polymerase chain reaction and Western blot analysis. The in vivo antitumorigenic activities of WE, SF, and NSF were investigated in a xenograft mouse model. Results: SF induced apoptotic death of C6 glioma cells and suppressed migration and proliferation of C6 glioma cells, whereas WE and NSF neither induced apoptosis nor suppressed migration of C6 glioma cells. SF downregulated the expression of the anti-apoptotic gene B-cell lymphoma-2 (Bcl-2) and upregulated the expression of the pro-apoptotic gene Bcl-2-associated X protein (BAX) in C6 glioma cells but had no effect on the expression of the p53 tumor-suppressor gene. Moreover, SF treatment resulted in activation of caspase-3 as evidenced by increased levels of cleaved caspase-3. Finally, WE, SF, and NSF exhibited in vivo antitumorigenic activities in the xenograft mouse model by suppressing the growth of grafted CT-26 carcinoma cells without decreasing the animal body weight. Conclusion: These results suggest that WE, SF, and NSF of KRG are able to suppress tumor growth via different molecular and cellular mechanisms, including induction of apoptosis and activation of immune cells. (C) 2017 The Korean Society of Ginseng, Published by Elsevier Korea LLC. This is an open access article under the CC BY-NC-ND license.
引用
收藏
页码:386 / 391
页数:6
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