Neuroprotective Effects of 3α-Acetoxyeudesma-1,4(15),11(13)-trien-12,6α-olide Against Dopamine-Induced Apoptosis in the Human Neuroblastoma SH-SY5Y Cell Line

被引:0
作者
Uk Koo
Kung-Woo Nam
Ahrom Ham
Dahyun Lyu
Bora Kim
Sung-Jin Lee
Kyeong Ho Kim
Ki-Bong Oh
Woongchon Mar
Jongheon Shin
机构
[1] College of Pharmacy,Natural Products Research Institute
[2] Seoul National University,Department of Neuroscience, College of Medicine
[3] Korea University,Department of Animal Biotechnology
[4] Kangwon National University,College of Pharmacy
[5] Kangwon National University,Department of Agricultural Biotechnology College of Agriculture and Life Science
[6] Seoul National University,undefined
来源
Neurochemical Research | 2011年 / 36卷
关键词
3α-acetoxyeudesma-1; 4(15); 11(13)-trien-12; 6α-olide; Tyrosinase activity; Dopamine; Apoptosis; Quinoprotein; α-synuclein;
D O I
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中图分类号
学科分类号
摘要
Dopamine (DA), as a neurotoxin, can elicit severe Parkinson’s disease-like syndrome by elevating intracellular reactive oxygen species (ROS) levels and apoptotic activity. We examined the inhibitory effects of 3α-acetoxyeudesma-1,4(15),11(13)-trien-12,6α-olide (AETO), purified from the leaves of Laurus nobilis L., on DA-induced apoptosis and α-synuclein (α-syn) formation in dopaminergic SH-SY5Y cells. AETO decreased the active form of caspase-3 and the levels of p53, which were accompanied by increased levels of Bcl-2 in a dose-dependent manner. Flow cytometric and Western blot analysis showed that AETO significantly inhibited DA-induced apoptosis along with suppression of intracellular tyrosinase activity, ROS generation, quinoprotein, and α-syn formation (P < 0.01). These results indicate that AETO inhibited DA-induced apoptosis, which is closely related to the suppression of intracellular tyrosinase activity and the formation of α-syn, ROS, and quinoprotein in SH-SY5Y cells.
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页码:1991 / 2001
页数:10
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共 162 条
[1]  
Bonnet AM(1999)Pathophysiology of Parkinson’s disease Biomed Pharmacother 53 117-121
[2]  
Houeto JL(1999)Etiology and pathogenesis of Parkinson’s disease Annu Rev Neurosci 22 123-144
[3]  
Olanow CW(1993)A radical hypothesis for neurodegeneration Trends Neurosci 16 439-444
[4]  
Tatton WG(2001)Apoptotic signaling in dopamine-induced cell death: the role of oxidative stress, p38 mitogen-activated protein kinase, cytochrome c and caspases J Neurochem 78 374-383
[5]  
Olanow CW(1978)Oxidative pathways for catecholamines in the genesis of neuromelanin and cytotoxic quinones Mol Pharmacol 14 633-643
[6]  
Junn E(1974)The generation of hydrogen peroxide, superoxide radical, and hydroxyl radical by 6-hydroxydopamine, dialuric acid, and related cytotoxic agents J Biol Chem 249 2447-2452
[7]  
Mouradian MM(1995)Enzymatic oxidation of dopamine: the role of prostaglandin H synthase J Neurochem 64 919-924
[8]  
Graham DG(1992)Reactive oxygen species and the central nervous system J Neurochem 59 1609-1623
[9]  
Cohen G(2000)Drug treatment of Parkinson’s disease. Time for phase II Biochem Pharmacol 59 1023-1031
[10]  
Heikkila RE(1997)Dopamine synthesis, uptake, metabolism, and receptors: relevance to gene therapy of Parkinson’s disease Exp Neurol 144 4-9