Neuroprotective Effect of Honokiol and Magnolol, Compounds from Magnolia officinalis, on Beta-amyloid-induced Toxicity in PC12 Cells

被引:133
作者
Hoi, Chu Peng [1 ]
Ho, Yee Ping [1 ]
Baum, Larry [1 ]
Chow, Albert H. L. [1 ]
机构
[1] Chinese Univ Hong Kong, Sch Pharm, Shatin, Hong Kong, Peoples R China
关键词
A beta; neurotoxicity; Alzheimer's disease; neuroprotective; calcium; apoptosis; ALZHEIMERS-DISEASE; OXIDATIVE STRESS; CALCIUM HOMEOSTASIS; PRECURSOR PROTEIN; INDUCED APOPTOSIS; DEATH; ACTIVATION; CASPASE-3; SURVIVAL; PEPTIDE;
D O I
10.1002/ptr.3178
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Amyloid beta peptide (A beta) induced toxicity is a well-established pathway of neuronal cell death which might play a role in Alzheimer's disease. In this regard, the toxic effect of A beta on a cultured A beta-sensitive neuronal cell line was used as a primary screening tool for potential anti-Alzheimer's therapeutic agents. The effects of nine pure compounds (vitamin E, alpha-asarone, salidroside, baicolin, magnolol, gastrodin, bilobalide, honokiol and beta-asarone) from selected Chinese herbs on neuronal cell death induced by A beta in NGF-differentiated PC12 cells were examined. Only two of the studied compounds, honokiol and magnolol, significantly decreased A beta-induced cell death. Further experiments indicated that their neuroprotective effects are possibly mediated through reduced ROS production as well as suppression of intracellular calcium elevation and inhibition of caspase-3 activity. The results provide for the first time a scientific rationale for the clinical use of honokiol and magnolol in the treatment of Alzheimer's disease. Copyright (c) 2010 John Wiley & Sons, Ltd.
引用
收藏
页码:1538 / 1542
页数:5
相关论文
共 29 条
[1]  
Bayer TA, 2001, BRAIN PATHOL, V11, P1
[2]   VITAMIN-E PROTECTS NERVE-CELLS FROM AMYLOID BETA-PROTEIN TOXICITY [J].
BEHL, C ;
DAVIS, J ;
COLE, GM ;
SCHUBERT, D .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1992, 186 (02) :944-950
[3]   HYDROGEN-PEROXIDE MEDIATES AMYLOID-BETA PROTEIN TOXICITY [J].
BEHL, C ;
DAVIS, JB ;
LESLEY, R ;
SCHUBERT, D .
CELL, 1994, 77 (06) :817-827
[4]   Neuronal cell death and reactive oxygen species [J].
Boldyrev, A ;
Song, RJ ;
Dyatlov, VA ;
Lawrence, DA ;
Carpenter, DO .
CELLULAR AND MOLECULAR NEUROBIOLOGY, 2000, 20 (04) :433-450
[5]   THE CA2+ INFLUX INDUCED BY BETA-AMYLOID PEPTIDE-25-35 IN CULTURED HIPPOCAMPAL-NEURONS RESULTS FROM NETWORK EXCITATION [J].
BRORSON, JR ;
BINDOKAS, VP ;
IWAMA, T ;
MARCUCCILLI, CJ ;
CHISHOLM, JC ;
MILLER, RJ .
JOURNAL OF NEUROBIOLOGY, 1995, 26 (03) :325-338
[6]   Therapeutic potential in Alzheimer disease [J].
Cash, AD ;
Perry, G ;
Smith, MA .
CURRENT MEDICINAL CHEMISTRY, 2002, 9 (17) :1605-1610
[7]   Mechanisms of neuronal death in Alzheimer's disease [J].
Cotman, CW ;
Su, JH .
BRAIN PATHOLOGY, 1996, 6 (04) :493-506
[8]  
DYRKS T, 1992, J BIOL CHEM, V267, P18210
[9]   Activation of caspase-3 in β-amyloid-induced apoptosis of cultured rat cortical neurons [J].
Harada, J ;
Sugimoto, M .
BRAIN RESEARCH, 1999, 842 (02) :311-323
[10]   Protective effect of S-allyl-L-cysteine, a garlic compound, on amyloid β-protein-induced cell death in nerve growth factor-differentiated PC12 cells [J].
Ito, Y ;
Kosuge, Y ;
Sakikubo, T ;
Horie, K ;
Ishikawa, N ;
Obokata, N ;
Yokoyama, E ;
Yamashina, K ;
Yamamoto, M ;
Saito, H ;
Arakawa, M ;
Ishige, K .
NEUROSCIENCE RESEARCH, 2003, 46 (01) :119-125