Neuroprotective effects of ginseng total saponin and ginsenosides Rb1 and Rg1 on spinal cord neurons in vitro

被引:224
作者
Liao, BS [1 ]
Newmark, H
Zhou, RP
机构
[1] Rutgers State Univ, Coll Pharm, Dept Biol Chem, Lab Canc Res, Piscataway, NJ 08854 USA
[2] Robert Wood Johnson Med Sch, Dept Neurosci & Cell Biol, Piscataway, NJ 08854 USA
关键词
neuroprotection; spinal cord injury; excitotoxicity; oxidative stress; neuron culture; ginseng total saponin; ginsenoside Rb1; ginsenoside Rg1; apoptosis; neurotrophic factors;
D O I
10.1006/exnr.2001.7841
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Spinal cord injury is a major cause of disability and results in many serious physical, psychological, and social difficulties. Numerous studies have shown that traumatic spinal cord injuries (SCI) lead to neuronal loss and axonal degeneration in and around the injury site that cause partial disability or complete paralysis. An important strategy in the treatment of SCI is to promote neuron survival and axon outgrowth, making possible the recovery of neural connections. Using an in vitro survival assay, we have identified ginsenosides Rb1 and Rg1, extracted from ginseng root (Panax ginseng C. A. Meyer), as efficient neuroprotective agents for spinal cord neurons. These compounds protect spinal neurons from excitotoxicity induced by glutamate and kainic acid, as well as oxidative stress induced by H2O2. The neuroprotective effects are dose-dependent. The optimal doses are 20-40 muM for ginsenosides Rb1 and Rg1. The effects are specific for Rb1 and Rg1, since a third ginsenoside, Re, did not exhibit any activity. Ginseng has been used for thousands of years in the treatment of neurological disorders and other diseases in Asia. Ginsenosides Rb1 and Rg1 represent potentially effective therapeutic agents for spinal cord injuries. (C) 2002 Elsevier Science (USA).
引用
收藏
页码:224 / 234
页数:11
相关论文
共 72 条
[1]   Impaired mitochondrial function, oxidative stress and altered antioxidant enzyme activities following traumatic spinal cord injury [J].
Azbill, RD ;
Mu, XJ ;
BruceKeller, AJ ;
Mattson, MP ;
Springer, JE .
BRAIN RESEARCH, 1997, 765 (02) :283-290
[2]   LIPID-PEROXIDATION IN EXPERIMENTAL SPINAL-CORD INJURY - TIME-LEVEL RELATIONSHIP [J].
BARUT, S ;
CANBOLAT, A ;
BILGE, T ;
AYDIN, Y ;
COKNESELI, B ;
KAYA, U .
NEUROSURGICAL REVIEW, 1993, 16 (01) :53-59
[3]   EFFECTS OF GINSENOSIDE-RB1 ON CENTRAL CHOLINERGIC METABOLISM [J].
BENISHIN, CG ;
LEE, R ;
WANG, LCH ;
LIU, HJ .
PHARMACOLOGY, 1991, 42 (04) :223-229
[4]   APOPTOSIS AND NECROSIS - 2 DISTINCT EVENTS INDUCED, RESPECTIVELY, BY MILD AND INTENSE INSULTS WITH N-METHYL-D-ASPARTATE OR NITRIC-OXIDE SUPEROXIDE IN CORTICAL CELL-CULTURES [J].
BONFOCO, E ;
KRAINC, D ;
ANKARCRONA, M ;
NICOTERA, P ;
LIPTON, SA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (16) :7162-7166
[5]   NT-3 promotes growth of lesioned adult rat sensory axons ascending in the dorsal columns of the spinal cord [J].
Bradbury, EJ ;
Khemani, S ;
King, VR ;
Priestley, JV ;
McMahon, SB .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1999, 11 (11) :3873-3883
[6]  
BRAUGHLER JM, 1988, J PHARMACOL EXP THER, V244, P423
[7]   NEW SUBSTANCES OF PLANT ORIGIN WHICH INCREASE NONSPECIFIC RESISTANCE [J].
BREKHMAN, II ;
DARDYMOV, IV .
ANNUAL REVIEW OF PHARMACOLOGY, 1969, 9 :419-&
[9]   NEUROANATOMICAL ANALYSIS OF SPINAL-CORD INJURY IN RHESUS-MONKEY (MACACA-MULATTA) [J].
BRESNAHAN, JC ;
KING, JS ;
MARTIN, GF ;
YASHON, D .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 1976, 28 (04) :521-542
[10]   EXCITOTOXIC CELL-DEATH [J].
CHOI, DW .
JOURNAL OF NEUROBIOLOGY, 1992, 23 (09) :1261-1276