New triterpenoid from Panax ginseng exhibits cytotoxicity through p53 and the caspase signaling pathway in the HepG2 cell line

被引:19
作者
Huang, Jian [1 ,2 ]
Tang, Xiao-hui [1 ]
Ikejima, Takashi [2 ]
Sun, Xiu-jia [3 ]
Wang, Xiao-bo [4 ]
Xi, Rong-gang [4 ]
Wu, Li-jun [1 ]
机构
[1] Shenyang Pharmaceut Univ, Dept Phytochem, Shenyang 110016, Peoples R China
[2] Shenyang Pharmaceut Univ, China Japan Res Inst Med & Pharmaceut Sci, Shenyang 110016, Peoples R China
[3] Qiqihar Univ, Sch Chem, Qiqihar 161006, Peoples R China
[4] 210th Hosp People Liberat Army, Dept Tradit Chinese Med, Shool Pharm, Shenli Roa, Peoples R China
关键词
Panax ginseng; triterpenoid; cytotoxicity; HepG2; cell cycle; p53; caspase;
D O I
10.1007/s00000-001-1159-8
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
A new triterpenoid, 20(R),22(),24(S)-dammar-25(26)-ene-3 beta,6 alpha,12 beta,20,22,24-hexanol (1), and three known triterpenoids, beta-D-glucopyranoside,(3 beta,12 beta)-12,20-dihydroxydammar-24-en3-yl,6-acetate (2), 20(R)-ginsenoside Rg(3)(3), and 20(R)-ginsenoside Rh-2(4), were isolated from the leaves of Panax ginseng. Their structures were determined by chemical analysis and spectral methods (IR, 1D and 2D NMR, HR-ESI-MS). Compounds 1-4 were exhibited various degrees of cytotoxicity in the human hepatoma cell line, HepG2. Compound 1 had the highest cytotoxic potency, with an IC50 value of 20.1 mu M, by stimulating p53-mediated cell cycle arrest at the G1 to S phase transition, leading to apoptosis via activation of the caspase signaling pathway.
引用
收藏
页码:323 / 329
页数:7
相关论文
共 26 条
[11]   Pan-caspase inhibitor zVAD enhances cell death in RAW246.7 macrophages [J].
Kim, SO ;
Han, JH .
JOURNAL OF ENDOTOXIN RESEARCH, 2001, 7 (04) :292-296
[12]   CHEMICAL STUDIES ON CRUDE DRUG PRECESSION .1. ON THE CONSTITUENTS OF GINSENG RADIX RUBRA [J].
KITAGAWA, I ;
YOSHIKAWA, M ;
YOSHIHARA, M ;
HAYASHI, T ;
TANIYAMA, T .
YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN, 1983, 103 (06) :612-622
[13]  
LANE DP, 1992, NATURE, V358, P16
[14]  
Lee JH, 2002, INT J ONCOL, V21, P1239
[15]  
Ma Shuang-gang, 2005, Yaoxue Xuebao, V40, P924
[16]   Death signal-induced localization of p53 protein to mitochondria - A potential role in apoptotic signaling [J].
Marchenko, ND ;
Zaika, A ;
Moll, UM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (21) :16202-16212
[17]  
MIYASHITA T, 1995, CELL, V80, P293
[18]   Imaging of caspase-3 activation in HeLa cells stimulated with etoposide using a novel fluorescent probe [J].
Mizukami, S ;
Kikuchi, K ;
Higuchi, T ;
Urano, Y ;
Mashima, T ;
Tsuruo, T ;
Nagano, T .
FEBS LETTERS, 1999, 453 (03) :356-360
[19]   IDENTIFICATION AND INHIBITION OF THE ICE/CED-3 PROTEASE NECESSARY FOR MAMMALIAN APOPTOSIS [J].
NICHOLSON, DW ;
ALI, A ;
THORNBERRY, NA ;
VAILLANCOURT, JP ;
DING, CK ;
GALLANT, M ;
GAREAU, Y ;
GRIFFIN, PR ;
LABELLE, M ;
LAZEBNIK, YA ;
MUNDAY, NA ;
RAJU, SM ;
SMULSON, ME ;
YAMIN, TT ;
YU, VL ;
MILLER, DK .
NATURE, 1995, 376 (6535) :37-43
[20]  
QIU F, 2007, CHIN J MED CHEM, V8, P205