Rosmarinic Acid Antagonized 1-Methyl-4-Phenylpyridinium (MPP+)-Induced Neurotoxicity in MES23.5 Dopaminergic Cells

被引:33
作者
Du, Tingting [1 ,2 ]
Li, Lu [1 ,2 ]
Song, Ning [1 ,2 ]
Xie, Junxia [1 ,2 ]
Jiang, Hong [1 ,2 ]
机构
[1] Qingdao Univ, Coll Med, Shandong Prov Key Lab Pathogenesis & Prevent Neur, Dept Physiol, Qingdao 266071, Peoples R China
[2] Qingdao Univ, Coll Med, State Key Disciplines Physiol, Qingdao 266071, Peoples R China
关键词
rosmarinic acid; MPP+; Parkinson's disease; apoptosis; PARKINSONS-DISEASE; INDUCED APOPTOSIS; OXIDATIVE STRESS; SUBSTANTIA-NIGRA; MECHANISM; DEATH; ASTROCYTES; NEURONS; MODEL;
D O I
10.1177/1091581810383705
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Rosmarinic acid (RA) is a naturally occurring polyphenolic compound found in various plant families. We previously reported that RA exerted protective effects against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity through antioxidative properties. In this study, we investigated whether RA could prevent effects of 1-methyl-4-phenylpyridinium (MPP+)-induced insult in MES23.5 dopamineric cells. 1-Methyl-4-phenylpyridinium treatment decreased cell viability and dopamine content, as well as caused apoptotic morphological changes. 1-Methyl-4-phenylpyridinium-induced mitochondrial dysfunction, indicated by inhibition of activity associated with mitochondrial respiratory chain complex 1, suggested mitochondrial transmembrane potential collapse and generation of reactive oxygen species. Decreased Bcl-2/Bax ratio and caspase 3 activation were also observed. Rosmarinic acid pretreatment restored the complex 1 activity of the mitochondrial respiratory chain and partially reversed the other damaging effects of MPP+. Our results indicate that RA plays a neuroprotective role by ameliorating mitochondrial dysfunction against MPP+-induced cell apoptosis and suggest that RA has the potential to be considered an aid for prevention of Parkinson's disease.
引用
收藏
页码:625 / 633
页数:9
相关论文
共 37 条
[1]   Neurodegenerative diseases and oxidative stress [J].
Barnham, KJ ;
Masters, CL ;
Bush, AI .
NATURE REVIEWS DRUG DISCOVERY, 2004, 3 (03) :205-214
[2]   Cell death in the nervous system [J].
Bredesen, Dale E. ;
Rao, Rammohan V. ;
Mehlen, Patrick .
NATURE, 2006, 443 (7113) :796-802
[3]   Death receptors couple to both cell proliferation and apoptosis [J].
Budd, RC .
JOURNAL OF CLINICAL INVESTIGATION, 2002, 109 (04) :437-441
[4]   Mitochondria and neuronal death/survival signaling pathways in cerebral ischemia [J].
Chan, PH .
NEUROCHEMICAL RESEARCH, 2004, 29 (11) :1943-1949
[5]  
CRAWFORD GD, 1992, J NEUROSCI, V12, P3392
[6]   Parkinson's disease: Mechanisms and models [J].
Dauer, W ;
Przedborski, S .
NEURON, 2003, 39 (06) :889-909
[7]   Ghrelin Antagonized 1-Methyl-4-Phenylpyridinium (MPP+)-Induced Apoptosis in MES23.5 Cells [J].
Dong, Juanjuan ;
Song, Ning ;
Xie, Junxia ;
Jiang, Hong .
JOURNAL OF MOLECULAR NEUROSCIENCE, 2009, 37 (02) :182-189
[8]   Description of Parkinson's disease as a clinical syndrome [J].
Fahn, S .
PARKINSON'S DISEASE: THE LIFE CYCLE OF THE DOPAMINE NEURON, 2003, 991 :1-14
[9]  
Gao LP, 2005, PHARMAZIE, V60, P62
[10]   Neuroinflammatory processes in Parkinson's disease [J].
Hunot, S ;
Hirsch, EC .
ANNALS OF NEUROLOGY, 2003, 53 :S49-S58