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论文类型：期刊论文

发表时间：2009-12-01

发表刊物：NEUROCHEMISTRY INTERNATIONAL

收录刊物：SCIE、PubMed、Scopus

卷号：55

期号：8

页面范围：741-746

ISSN号：0197-0186

关键字：Catalpol; A beta(1-42); Caspase; Cortical neurons; Mitochondria

摘要：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.