Bicyclol attenuates oxidative stress and neuronal damage following transient forebrain ischemia in mouse cortex and hippocampus.

Abstract

To assess its potential neuroprotective effect against ischemia/reperfusion (IR) injury in mice, bicyclol was administered intragastrically once a day for 3 days. After 6h of bicyclol pretreatment on the third day, forebrain ischemia was induced for 1h by bilateral occlusion of the carotid arteries. After different times of reperfusion, the histopathological changes and the levels of mitochondria-generated reactive oxygen species (ROS), malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in the cortex and hippocampus were measured. We found that extensive neuronal death occurred in the cortex and the CA1 area of the hippocampus at day 7 after IR and that bicyclol significantly attenuated IR-induced neuronal death in a dose-dependent manner. We also found that pretreatment with bicyclol dose dependently decreased the generation of ROS and the MDA content and reduced the compensatory increase in SOD activity in the cortex and hippocampus at 4h of reperfusion. These results suggest that bicyclol protects the mouse brain against cerebral IR injury by attenuating oxidative stress and lipid peroxidation.

• Authors: Li-Na Sun, Jia Shen, Fang Su, Qian Wang, Yu-Jin Zhu, Xiao-E Lou, Hua-Wei Liang, Iain C Bruce, Qiang Xia
• Journal: Neuroscience letters (Neurosci Lett) Vol. 459 Issue 2 Pg. 84-7 (Aug 07 2009) ISSN: 1872-7972 [Electronic] Ireland
• PMID: 19427356 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Biphenyl Compounds
• Neuroprotective Agents
• Reactive Oxygen Species
• Malondialdehyde
• bicyclol
• Superoxide Dismutase

Topics

• Animals
• Biphenyl Compounds (administration & dosage)
• Brain Ischemia (drug therapy, metabolism, pathology)
• Cell Count
• Cell Death (drug effects)
• Cell Survival (drug effects)
• Cerebral Cortex (drug effects, metabolism, pathology)
• Dose-Response Relationship, Drug
• Hippocampus (drug effects, metabolism, pathology)
• Male
• Malondialdehyde (metabolism)
• Mice
• Mice, Inbred ICR
• Mitochondria (metabolism)
• Neurons (drug effects, pathology)
• Neuroprotective Agents (administration & dosage)
• Oxidative Stress (drug effects)
• Reactive Oxygen Species (metabolism)
• Reperfusion Injury (drug therapy, metabolism, pathology)
• Superoxide Dismutase (metabolism)