title: Procyanidins protects against oxidative damage and cognitive deficits after traumatic brain injury.
abstract: OBJECTIVE
  Oxidative stress is the principal factor in traumatic brain injury (TBI) that initiates the events that result in protracted neuronal dysfunction and remodeling. Importantly, antioxidants can protect the brain against oxidative damage and modulate the capacity of the brain to cope with synaptic dysfunction and cognitive impairment.
  
  
  METHODS
  To date, however, no studies have investigated the effects of procyanidins (PC) on cognitive deficits after TBI.
  
  
  METHODS
  In the present study, rats with controlled cortical impact (CCI) were used to investigate the protective effects of procyanidins.
  
  
  RESULTS
  The results showed that procyanidins reduced the level of malondialdehyde (MDA) and elevated the level of glutathione (GSH) and the activity of superoxide dismutase (SOD). In addition, treatment with procyanidins, which elevated the levels of brain-derived neurotropic factor (BDNF), phosphorylation-cAMP-response element binding protein (pCREB), total CREB, and cyclic AMP (cAMP), improved cognitive performance in the Morris water maze after TBI.
  
  
  CONCLUSIONS
  These results suggest that procyanidins appear to counteract oxidative damage and behavioral dysfunction after TBI through antioxidant activity and the up-regulation of cAMP/CREB signaling.
authors.affiliation: a Department of Neurosurgery , The First Affiliated Hospital of Anhui Medical University , No. 218 Jixi Road, Shushan District , Hefei, Anhui , People's Republic of China .
authors.forename: Xiang
authors.initials: X
authors.lastname: Mao
authors.forename: Shuyu
authors.initials: S
authors.lastname: Hao
authors.forename: Zhendan
authors.initials: Z
authors.lastname: Zhu
authors.forename: Hao
authors.initials: H
authors.lastname: Zhang
authors.forename: Weichuan
authors.initials: W
authors.lastname: Wu
authors.forename: Feifan
authors.initials: F
authors.lastname: Xu
authors.forename: Baiyun
authors.initials: B
authors.lastname: Liu
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001930:Brain Injuries / Q000188:drug therapy* / Q000378:metabolism*; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D003072:Cognition Disorders / Q000188:drug therapy* / Q000378:metabolism*; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018782:Maze Learning / Q000187:drug effects; D009473:Neuronal Plasticity / Q000502:physiology; D018384:Oxidative Stress / Q000187:drug effects*; D044945:Proanthocyanidins / Q000494:pharmacology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D019208:Brain-Derived Neurotrophic Factor; D017362:Cyclic AMP Response Element-Binding Protein; D044945:Proanthocyanidins; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D005978:Glutathione
keywords: Antioxidant; CREB; TBI; hippocampus; oxidative stress; procyanidins