期刊
NEUROCHEMISTRY INTERNATIONAL
卷 55, 期 8, 页码 741-746出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2009.07.004
关键词
Catalpol; A beta(1-42); Caspase; Cortical neurons; Mitochondria
资金
- Natural Science Foundation of Liaoning [20072185]
- Science and Technology Project of Dalian [2008E11SF163]
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 LIPS, MPP+ and rotenone. Here, we further evaluated the effect of catalpol against A beta(1-42)-induced apoptosis in primary cortical neuron cultures. In the present study, the primary cortical neuron culture treated with A beta(1-42) Was severed as cell model of Alzheimer's disease (AD) in vitro. By exposure to A beta(1-42) (5 mu M) 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 (0.5 mM) for 30 min prior to A beta(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 A beta(1-42) through a mitochondrial-dependent caspase pathway. (C) 2009 Elsevier Ltd. Ail rights reserved.
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