title: Bone morphogenetic protein-7 ameliorates cerebral ischemia and reperfusion injury via inhibiting oxidative stress and neuronal apoptosis.
abstract: Previous studies have indicated that bone morphogenetic protein-7 (BMP-7) is neuroprotective against cerebral ischemia/reperfusion (IR) injury. The present study was undertaken to determine the molecular mechanisms involved in this effect. Adult male Wistar rats were subjected to 2 h of transient middle cerebral artery occlusion (MCAO), followed by 24 h of reperfusion. BMP-7 (10-4 g/kg) or vehicle was infused into rats at the onset of reperfusion via the tail vein. Neurological deficits, infarct volume, histopathological changes, oxidative stress-related biochemical parameters, neuronal apoptosis, and apoptosis-related proteins were assessed. BMP-7 significantly improved neurological and histological deficits, reduced the infarct volume, and decreased apoptotic cells after cerebral ischemia. BMP-7 also markedly enhanced the activities of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), and reduced the level of malondialdehyde (MDA) in IR rats. In addition, Western blot analysis indicated that BMP-7 prevented cytochrome c release, inhibited activation of caspase-3, caspase-9 and caspase-8. Our data suggested that BMP-7 has protective effects against cerebral IR injury in rats, and the neuroprotective effects may be attributed to attenuating oxidative stress and inhibiting neuronal apoptosis.
authors.affiliation: Department of Neurology, Affiliated Hospital of Medical College Qingdao University, Qingdao 266003, Shandong, China. guoqdsd@163.com.
authors.forename: Haitao
authors.initials: H
authors.lastname: Pei
authors.forename: Dongming
authors.initials: D
authors.lastname: Cao
authors.forename: Zhuangli
authors.initials: Z
authors.lastname: Guo
authors.forename: Guofang
authors.initials: G
authors.lastname: Liu
authors.forename: Yunliang
authors.initials: Y
authors.lastname: Guo
authors.forename: Chenglong
authors.initials: C
authors.lastname: Lu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D055419:Bone Morphogenetic Protein 7 / Q000494:pharmacology*; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology; D053148:Caspase 3 / Q000378:metabolism; D053181:Caspase 8 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D045304:Cytochromes c / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009474:Neurons / Q000166:cytology / Q000187:drug effects; D018696:Neuroprotective Agents / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D055419:Bone Morphogenetic Protein 7; D018696:Neuroprotective Agents; D008315:Malondialdehyde; D045304:Cytochromes c; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D053148:Caspase 3; D053181:Caspase 8; D053453:Caspase 9