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Indexed by:期刊论文

Date of Publication:2008-02-01

Journal:NEUROLOGICAL RESEARCH

Included Journals:SCIE、PubMed

Volume:30

Issue:1

Page Number:106-112

ISSN No.:0161-6412

Key Words:Bcl-2; caspase-3; catalpol; ischemia; PC12; ROS

Abstract:Objectives: Catalpol has been identified to have neuroprotective effect on gerbils subjected to transient global cerebral ischemia. However, the mechanism that catalpol prevents ischemia is still unclear. In the present study, PC12 cells, exposed to oxygen and glucose deprivation (OGD) followed by reperfusion, were used as an in vitro model of ischemia. The protective effects of catalpol were investigated in ischemic-induced apoptosis in PC72 cells.
   Methods: After OGD for 3 hours and reoxygenation for 18 hours, cell survival was quantified by the reduction of 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) were determined using commercially available kits. Caspase-3 assay was performed using caspase-3 assay kit. Microplate reader was used to detect the intensities of rhodamine123 (Rh123) and reactive oxygen species (ROS). The level of Bcl-2 protein was measured by flow cytometry.
   Results: Catalpol attenuated ischemia-induced apoptotic death via preventing the decrease in the level of Bcl-2 protein and the activities of SOD and GSH-PX, inhibiting the reduction of mitochondrial membrane potential and suppressing activation of caspase-3.
   Discussion: The results suggest that the catalpol has the potential to prevent ischemic-induced apoptosis.