Catalpol protects primary cultured cortical neurons induced by Abeta(1-42) through a mitochondrial-dependent caspase pathway.
Neurochem Int
; 55(8): 741-6, 2009 Dec.
Article
en En
| MEDLINE
| ID: mdl-19631247
ABSTRACT
It has been reported that catalpol, an iridoid glucoside, isolated from the root of Rehmannia glutinosa, protected cells from damage induced by a variety of toxic stimulus such as LPS, MPP(+) and rotenone. Here, we further evaluated the effect of catalpol against Abeta(1-42)-induced apoptosis in primary cortical neuron cultures. In the present study, the primary cortical neuron culture treated with Abeta(1-42) was severed as cell model of Alzheimer's disease (AD) in vitro. By exposure to Abeta(1-42) (5 microM) for 72 h in cultures, neuronal apoptosis occurred characterized by enhancement of activities of caspases and reactive oxygen species (ROS) as well as Bax increase, loss of mitochondrial membrane potential and cytochrome c release. Pretreatment with catalpol (0.5mM) for 30 min prior to Abeta(1-42) treatment attenuated neuronal apoptosis not only by reversing intracellular ROS accumulation, Bax level, mitochondrial membrane potential and, cytochrome c release to some extent, but also through regulating the activity and cleavage of caspase-3 and caspase-9. Thus, catalpol protects primary cultured cortical neurons induced by Abeta(1-42) through a mitochondrial-dependent caspase pathway.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Fragmentos de Péptidos
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Corteza Cerebral
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Péptidos beta-Amiloides
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Fármacos Neuroprotectores
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Caspasas
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Compuestos de Amonio Cuaternario
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Neuronas
Tipo de estudio:
Prognostic_studies
Idioma:
En
Revista:
Neurochem Int
Año:
2009
Tipo del documento:
Article
País de afiliación:
China