Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6023016 | Neurobiology of Disease | 2009 | 6 Pages |
Abstract
Ischemic preconditioning (IPC) protects brain against ischemic injury by activating specific mechanisms. Our goal was to determine if the inducible heme oxygenase 1 (HO1) is required for such protection. IPC before transient or permanent ischemia reduced cortical infarct volumes by 57.4% and 33.9%, respectively at 48Â h in wildtype adult mice. Interestingly, IPC failed to protect the HO1 gene deleted mice against permanent ischemic brain injury. IPC also resulted in a significant increase in HO1 protein levels in the brain and correlated with reduced neurological deficits after permanent and transient brain ischemia. Our study demonstrates that neuroprotective effects of IPC are at least partially mediated via HO1. Elucidating the physiological/cellular role by which HO1 is protective against brain ischemia may aid the development of selective drugs to treat stroke and its associated neurological disorders.
Keywords
MCAHO1TMCAOpMCAOBCCAoTIAIPCCBFNDSTTCischemic preconditioningmiddle cerebral artery occlusionPermanent middle cerebral artery occlusiontransient middle cerebral artery occlusioncerebral blood flowtransient ischemic attackbilateral common carotid artery occlusionmiddle cerebral arteryNeuroprotectioncarbon monoxideNeurological deficit scorewildtypeheme oxygenase 1heme oxygenase
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Authors
Emil Zeynalov, Zahoor A. Shah, Rung-chi Li, Sylvain Doré,