| 19631247 |
Liang JH, Du J, Xu LD, Jiang T, Hao S, Bi J, Jiang B: Catalpol protects primary cultured cortical neurons induced by Abeta (1-42) through a mitochondrial-dependent caspase pathway. Neurochem Int. 2009 Dec;55(8):741-6. Epub 2009 Jul 22.
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. |
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