Catalpol protects primary cultured cortical neurons induced by Abeta(1-42) through a mitochondrial-dependent caspase pathway.

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.

• Authors: Jian Hua Liang, Jing Du, Lian Deng Xu, Tao Jiang, Shuang Hao, Jing Bi, Bo Jiang
• Journal: Neurochemistry international (Neurochem Int) Vol. 55 Issue 8 Pg. 741-6 (Dec 2009) ISSN: 1872-9754 [Electronic] England
• PMID: 19631247 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Amyloid beta-Peptides
• Neuroprotective Agents
• Peptide Fragments
• Quaternary Ammonium Compounds
• Reactive Oxygen Species
• amyloid beta-protein (1-42)
• bcl-2-Associated X Protein
• catamine AB
• Cytochromes c
• Caspase 3
• Caspase 9
• Caspases

Topics

• Alzheimer Disease (drug therapy, metabolism, physiopathology)
• Amyloid beta-Peptides (antagonists & inhibitors, toxicity)
• Animals
• Apoptosis (drug effects, physiology)
• Caspase 3 (drug effects, metabolism)
• Caspase 9 (drug effects, metabolism)
• Caspases (drug effects, metabolism)
• Cells, Cultured
• Cerebral Cortex (drug effects, metabolism, physiopathology)
• Cytochromes c (drug effects, metabolism)
• Drug Evaluation, Preclinical (methods)
• Energy Metabolism (drug effects, physiology)
• Membrane Potential, Mitochondrial (drug effects, physiology)
• Mice
• Mitochondria (drug effects, metabolism, pathology)
• Neurons (drug effects, metabolism, pathology)
• Neuroprotective Agents (pharmacology)
• Oxidative Stress (drug effects, physiology)
• Peptide Fragments (antagonists & inhibitors, toxicity)
• Quaternary Ammonium Compounds (pharmacology, therapeutic use)
• Reactive Oxygen Species (metabolism)
• bcl-2-Associated X Protein (drug effects, metabolism)