Sublethal cerebral ischemia inhibits caspase-3 activation induced by subsequent prolonged ischemia in the C57Black/Crj6 strain mouse
| Autor: | Hideyoshi Fujihara, Chaoran Wu, Tomohiro Yamakura, Ren-Zhi Zhan, Kiichiro Taga, Hiroshi Baba, Koki Shimoji, Sihua Qi |
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| Rok vydání: | 2001 |
| Předmět: |
Time Factors
Ratón Ischemia Caspase 3 Striatum Pharmacology Neuroprotection Brain Ischemia Brain ischemia Mice Prosencephalon Coumarins medicine Animals Ischemic Preconditioning Caspase Neurons biology business.industry General Neuroscience medicine.disease Caspase Inhibitors Corpus Striatum Enzyme Activation Mice Inbred C57BL Caspases Anesthesia Reperfusion biology.protein Ischemic preconditioning business |
| Zdroj: | Neuroscience Letters. 315:133-136 |
| ISSN: | 0304-3940 |
| DOI: | 10.1016/s0304-3940(01)02368-0 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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