Sublethal cerebral ischemia inhibits caspase-3 activation induced by subsequent prolonged ischemia in the C57Black/Crj6 strain mouse.

Abstract

Caspase-3 activation has been implicated in ischemic neuronal death. In the present study, we examined if cerebral ischemic tolerance induced by sublethal ischemia is associated with an attenuation of caspase-3 activation in a mouse forebrain ischemia model. Forebrain ischemia in C57Black/Crj6 strain mice was induced by bilateral common carotid artery occlusion (BCCAO) for 18 min. Two episodes of 6-min ischemia were carried out as preconditioning 48 and 72 h before the 18-min BCCAO. Caspase-3-like activity was determined by fluorescently monitoring the release of amino-4-methylcoumarin from N-acetyl-Asp-Glu-Val-Asp-7-amino-4-methylcoumarin in the striatal protein extracts at 4, 24, and 72 h after reperfusion. The results showed that the ischemic preconditioning significantly attenuated caspase-3 activation at 4, 24, and 72 h after reperfusion, and reduced neuronal loss caused by the 18-min ischemia as examined on the 7th day after reperfusion. The present results suggest that the neuroprotection achieved by ischemic preconditioning is related to an attenuation of caspase-3 activation.

• Authors: S Qi, R Z Zhan, C Wu, H Fujihara, T Yamakura, H Baba, K Taga, K Shimoji
• Journal: Neuroscience letters (Neurosci Lett) Vol. 315 Issue 3 Pg. 133-6 (Nov 27 2001) ISSN: 0304-3940 [Print] Ireland
• PMID: 11716981 (Publication Type: Journal Article)

Chemical References

• Caspase Inhibitors
• Coumarins
• Casp3 protein, mouse
• Caspase 3
• Caspases
• 7-amino-4-methylcoumarin

Topics

• Animals
• Brain Ischemia (enzymology, pathology)
• Caspase 3
• Caspase Inhibitors
• Caspases (metabolism)
• Corpus Striatum (metabolism)
• Coumarins (metabolism)
• Enzyme Activation
• Ischemic Preconditioning
• Mice
• Mice, Inbred C57BL
• Neurons (pathology)
• Prosencephalon (enzymology, pathology)
• Reperfusion
• Time Factors