Minocycline in phenotypic models of Huntington's disease

被引:49
|
作者
Bantubungi, K
Jacquard, C
Greco, A
Pintor, A
Chtarto, A
Tai, K
Galas, MC
Tenenbaum, L
Déglon, N
Popoli, P
Minghetti, L
Brouillet, E
Brotchi, J
Levivier, M
Scbiffmann, SN
Blum, D
机构
[1] Free Univ Brussels, Lab Expt Neurosurg, B-1070 Brussels, Belgium
[2] ULB Erasme, Neurophysiol Lab, Brussels, Belgium
[3] Serv Hosp Frederic Joliot, CEA, CNRS, URA 2210, Orsay, France
[4] Ist Super Sanita, Dept Cell Biol & Neurosci, Rome, Italy
[5] Ist Super Sanita, Dept Drug Res & Evaluat, Rome, Italy
[6] ULB Erasme, IRIBHN, Brussels, Belgium
[7] INSERM, U422, Lille, France
[8] CEA, Dept Med Res, Orsay, France
[9] CEA, ImaGene Program, Orsay, France
[10] ULB Erasme, Dept Neurosurg, Brussels, Belgium
关键词
Huntington's disease; 3-nitropropionic acid; quinolinic acid; minocycline; striatum; cell death;
D O I
10.1016/j.nbd.2004.09.017
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Minocycline has been shown to be neuroprotective in various models of neurodegenerative diseases. However, its potential in Huntington's disease (HD) models characterized by calpain-dependent degeneration and inflammation has not been investigated. Here, we have tested minocycline in phenotypic models of HD using 3-nitropropionic acid (3NP) intoxication and quinolinic acid (QA) injections. In the 3NP rat model, where the development of striatal lesions involves calpain, we found that minocycline was not protective, although it attenuated the development of inflammation induced after the onset of striatal degeneration. The lack of minocycline activity on calpain-dependent cell death was also confirmed in vitro using primary striatal cells. Conversely, we found that minocycline reduced lesions and inflammation induced by QA. In cultured cells, minocycline protected against mutated huntingtin and staurosporine, stimulations known to promote caspase-dependent cell death. Altogether, these data suggested that, in HD, minocycline may counteract the development of caspase-dependent neurodegeneration, inflammation, but not calpain-dependent neuronal death. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:206 / 217
页数:12
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