title: Prevention of inflammation is a mechanism of preconditioning-induced neuroprotection against focal cerebral ischemia.
abstract: A brief ischemic insult induces significant protection against subsequent massive ischemic events. The molecular mechanisms underlying this phenomenon known as preconditioning (PC)-induced ischemic tolerance are not completely understood. Inflammation seen during the acute phase after stroke is known to be detrimental to the neurological outcome. We presently evaluated if the neuroprotective actions of PC involves prevention of post-ischemic inflammation. Cohorts of adult rats were subjected to transient focal ischemia (60 min middle cerebral artery occlusion; MCAO), PC (10 min MCAO) and focal ischemia followed 72 h after PC. Prior PC significantly reduced the post-ischemic increased expression of many inflammatory genes including cytokines, chemokines, adhesion molecules and pro-inflammatory transcription factors, and prevented the infiltration of neutrophils and macrophages in the ipsilateral cortex of rats subjected to focal ischemia. PC also decreased the volume of infarction and neurological dysfunction caused by transient focal ischemia. These studies indicate that prevention of inflammation might be a contributing mechanism by which PC induces protection against focal ischemia.
authors.affiliation: Department of Neurological Surgery, University of Wisconsin, Madison, WI 53792, United States.
authors.forename: Kellie K
authors.initials: KK
authors.lastname: Bowen
authors.forename: Michelle
authors.initials: M
authors.lastname: Naylor
authors.forename: Raghu
authors.initials: R
authors.lastname: Vemuganti
mesh_terms: D000818:Animals; D001921:Brain / Q000098:blood supply / Q000276:immunology / Q000503:physiopathology; D020520:Brain Infarction / Q000276:immunology / Q000503:physiopathology / Q000517:prevention & control; D002545:Brain Ischemia / Q000276:immunology* / Q000503:physiopathology / Q000628:therapy*; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism; D018925:Chemokines / Q000235:genetics / Q000378:metabolism; D002634:Chemotaxis, Leukocyte / Q000235:genetics / Q000276:immunology; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D019610:Cytoprotection / Q000276:immunology*; D004195:Disease Models, Animal; D004660:Encephalitis / Q000276:immunology* / Q000503:physiopathology / Q000517:prevention & control*; D005786:Gene Expression Regulation / Q000276:immunology; D020244:Infarction, Middle Cerebral Artery / Q000276:immunology / Q000503:physiopathology / Q000628:therapy; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism; D019194:Ischemic Preconditioning / Q000379:methods*; D008297:Male; D051381:Rats; D011918:Rats, Inbred SHR; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism
chemical_list: D015815:Cell Adhesion Molecules; D018925:Chemokines; D016207:Cytokines; D018836:Inflammation Mediators; D014157:Transcription Factors