title: Ischemic pre-conditioning preserves brain mitochondrial functions during the middle cerebral artery occlusion in rat.
abstract: It is well known that a brief period of ischemia increases tolerance to a subsequent severe ischemic episode. In the present study, bilateral carotid arteries occlusion (BCAO) was applied as pre-conditioning to testify whether this kind of ischemia could preserve the function of mitochondria with the impairment induced by middle cerebral artery occlusion (MCAO) in brain. The activities of respiratory enzyme complex I to IV, mitochondria swelling, membrane potential, and membrane fluidity were investigated. The results showed that the percentage of infarct area decreased greatly due to the ischemic pre-conditioning (IP) revealing the preventive effect of IP on infarct size. The activities of respiratory enzyme complex III, IV were effectively preserved (p < 0.05, p < 0.05) compared with MCAO group through ischemic pre-conditioning. Mitochondrial swelling and membrane fluidity were protected by IP, and also an increased trend was found in membrane potential, which indicated that the integrity of mitochondrial membrane was maintained. It suggested that the function of mitochondrial energy metabolism in brain ischemia was effectively protected by this kind of pre-conditioning.
authors.affiliation: National Center for Pharmaceutical Screening, Institute of Materia Medica, Peking Union Medical College, Chinese Academy of Medical Sciences, 1 XiangNongTan Street, Beijing 100050, China.
authors.forename: Hai-Xia
authors.initials: HX
authors.lastname: Zhang
authors.forename: Guan-Hua
authors.initials: GH
authors.lastname: Du
authors.forename: Jun-Tian
authors.initials: JT
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology; D002122:Calcium Chloride / Q000494:pharmacology; D016893:Carotid Stenosis / Q000378:metabolism / Q000473:pathology; D042967:Electron Transport Complex I; D042963:Electron Transport Complex II; D014450:Electron Transport Complex III / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000378:metabolism; D004734:Energy Metabolism / Q000502:physiology; D020244:Infarction, Middle Cerebral Artery / Q000378:metabolism* / Q000473:pathology; D019194:Ischemic Preconditioning; D008297:Male; D008560:Membrane Fluidity; D008564:Membrane Potentials; D008928:Mitochondria / Q000201:enzymology*; D008933:Mitochondrial Swelling; D009097:Multienzyme Complexes / Q000378:metabolism; D009247:NADH, NADPH Oxidoreductases / Q000378:metabolism; D010088:Oxidoreductases / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013385:Succinate Dehydrogenase / Q000378:metabolism
chemical_list: D009097:Multienzyme Complexes; D010088:Oxidoreductases; D042963:Electron Transport Complex II; D013385:Succinate Dehydrogenase; D009247:NADH, NADPH Oxidoreductases; D003576:Electron Transport Complex IV; D042967:Electron Transport Complex I; D014450:Electron Transport Complex III; D002122:Calcium Chloride