Nifedipine Prevents Iron Accumulation and Reverses Iron-Overload-Induced Dopamine Neuron Degeneration in the Substantia Nigra of Rats

被引:23
作者
Ma, ZeGang [1 ]
Zhou, Yu [1 ]
Xie, JunXia [1 ]
机构
[1] Qingdao Univ, Dept Physiol, Shandong Prov Key Lab Pathogenesis & Prevent Neur, Coll Med, Qingdao 266071, Peoples R China
关键词
Nifedipine; Iron; L-type Ca2+ channel; Dopamine neuron; PARKINSONS-DISEASE; CALCIUM-CHANNELS; NEURODEGENERATIVE DISORDERS; OXIDATIVE STRESS; CA2+ CHANNELS; BRAIN; CELLS; NEUROTOXICITY; MESENCEPHALON; LOCALIZATION;
D O I
10.1007/s12640-012-9309-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The mechanisms of iron accumulation in substantia nigra (SN) of Parkinson's diseases remain unclear. The objective of this study was to investigate effects of nifedipine on iron-overload-induced iron accumulation and neurodegeneration in SN of rats. By high performance liquid chromatography-electrochemical detection, tyrosine hydroxylase (TH) immunohistochemistry, and iron content array, we first quantified iron content and the number of dopamine neurons in SN of experimental rats treated with iron dextran. We further assessed effects of treatment with nifedipine. Our results showed that nifedipine treatment prevents iron dextran-induced dopamine depletion in the striatum. Consistently, we found that nifedipine restores the number of TH-positive neurons reduced by iron dextran overload and prevents increase of iron content in the SN. These results suggested that nifedipine may suppress iron toxicity in dopamine neurons and prevent neurodegeneration.
引用
收藏
页码:274 / 279
页数:6
相关论文
共 41 条
[1]   Microarray analysis of oxidative stress regulated genes in mesencephalic dopaminergic neuronal cells: Relevance to oxidation damage in Parkinson's disease [J].
Anantharam, Vellareddy ;
Lehrmann, Elin ;
Kanthasamy, Arthi ;
Yang, Yongjie ;
Banerjee, Probal ;
Becker, Kevin G. ;
Freed, William J. ;
Kanthasamy, Anumantha G. .
NEUROCHEMISTRY INTERNATIONAL, 2007, 50 (06) :834-847
[2]   Medical progress: Disorders of iron metabolism [J].
Andrews, NC .
NEW ENGLAND JOURNAL OF MEDICINE, 1999, 341 (26) :1986-1995
[3]   Iron metabolism in parkinsonian syndromes [J].
Berg, Daniela ;
Hochstrasser, Helmine .
MOVEMENT DISORDERS, 2006, 21 (09) :1299-1310
[4]   Molecular pathways involved in the neurotoxicity of 6-OHDA, dopamine and MPTP: contribution to the apoptotic theory in Parkinson's disease [J].
Blum, D ;
Torch, S ;
Lambeng, N ;
Nissou, MF ;
Benabid, AL ;
Sadoul, R ;
Verna, JM .
PROGRESS IN NEUROBIOLOGY, 2001, 65 (02) :135-172
[5]  
Bradbury MWB, 1997, J NEUROCHEM, V69, P443
[6]   'Rejuvenation' protects neurons in mouse models of Parkinson's disease [J].
Chan, C. Savio ;
Guzman, Jaime N. ;
Ilijic, Ema ;
Mercer, Jeff N. ;
Rick, Caroline ;
Tkatch, Tatiana ;
Meredith, Gloria E. ;
Surmeier, D. James .
NATURE, 2007, 447 (7148) :1081-U5
[7]  
De Waard M, 1996, Ion Channels, V4, P41
[8]   INCREASED NIGRAL IRON CONTENT AND ALTERATIONS IN OTHER METAL-IONS OCCURRING IN BRAIN IN PARKINSONS-DISEASE [J].
DEXTER, DT ;
WELLS, FR ;
LEES, AJ ;
AGID, F ;
AGID, Y ;
JENNER, P ;
MARSDEN, CD .
JOURNAL OF NEUROCHEMISTRY, 1989, 52 (06) :1830-1836
[9]   Neuromelanin associated redox-active iron is increased in the substantia nigra of patients with Parkinson's disease [J].
Faucheux, BA ;
Martin, ME ;
Beaumont, C ;
Hauw, JJ ;
Agid, Y ;
Hirsch, EC .
JOURNAL OF NEUROCHEMISTRY, 2003, 86 (05) :1142-1148
[10]   Blood vessels change in the mesencephalon of patients with Parkinson's disease [J].
Faucheux, BA ;
Bonnet, AM ;
Agid, Y ;
Hirsch, EC .
LANCET, 1999, 353 (9157) :981-982