PMID- 25279568 OWN - NLM STAT- MEDLINE DCOM- 20160621 LR - 20150819 IS - 1362-301X (Electronic) IS - 0269-9052 (Linking) VI - 29 IP - 1 DP - 2015 TI - Procyanidins protects against oxidative damage and cognitive deficits after traumatic brain injury. PG - 86-92 LID - 10.3109/02699052.2014.968621 [doi] AB - PRIMARY 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. RESEARCH DESIGN: To date, however, no studies have investigated the effects of procyanidins (PC) on cognitive deficits after TBI. METHODS AND PROCEDURES: In the present study, rats with controlled cortical impact (CCI) were used to investigate the protective effects of procyanidins. MAIN OUTCOMES AND 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. FAU - Mao, Xiang AU - Mao X AD - 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 . FAU - Hao, Shuyu AU - Hao S FAU - Zhu, Zhendan AU - Zhu Z FAU - Zhang, Hao AU - Zhang H FAU - Wu, Weichuan AU - Wu W FAU - Xu, Feifan AU - Xu F FAU - Liu, Baiyun AU - Liu B LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Brain Inj JT - Brain injury JID - 8710358 RN - 0 (Antioxidants) RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Cyclic AMP Response Element-Binding Protein) RN - 0 (Proanthocyanidins) RN - 4Y8F71G49Q (Malondialdehyde) RN - EC 1.15.1.1 (Superoxide Dismutase) RN - GAN16C9B8O (Glutathione) SB - IM MH - Animals MH - Antioxidants/pharmacology MH - Brain Injuries/*drug therapy/*metabolism MH - Brain-Derived Neurotrophic Factor/metabolism MH - Cognition Disorders/*drug therapy/*metabolism MH - Cyclic AMP Response Element-Binding Protein/metabolism MH - Glutathione/metabolism MH - Male MH - Malondialdehyde/metabolism MH - Maze Learning/drug effects MH - Neuronal Plasticity/physiology MH - Oxidative Stress/*drug effects MH - Proanthocyanidins/*pharmacology MH - Random Allocation MH - Rats MH - Rats, Sprague-Dawley MH - Superoxide Dismutase/metabolism OTO - NOTNLM OT - Antioxidant OT - CREB OT - TBI OT - hippocampus OT - oxidative stress OT - procyanidins EDAT- 2014/10/04 06:00 MHDA- 2016/06/22 06:00 CRDT- 2014/10/04 06:00 PHST- 2014/10/04 06:00 [entrez] PHST- 2014/10/04 06:00 [pubmed] PHST- 2016/06/22 06:00 [medline] AID - 10.3109/02699052.2014.968621 [doi] PST - ppublish SO - Brain Inj. 2015;29(1):86-92. doi: 10.3109/02699052.2014.968621.