title: Exercise ameliorates cognition impairment due to restraint stress-induced oxidative insult and reduced BDNF level.
abstract: We assessed whether chronic treadmill exercise attenuated restraint stress-induced cognition impairment. Although serum corticosterone was not significantly altered by exercise, the restraint-induced increases in hippocampal malondialdehyde (MDA) and 4-hydroxynonenal (HNE) were reduced by chronic exercise. The exercise paradigm also reversed stress-induced reductions in brain-derived neurotrophic factor (BDNF), which increased cAMP response element-binding protein (CREB) and AKT activation. We verified the relationship between oxidative stress and BDNF signaling by treating primary hippocampal cultures with hydrogen peroxide (H2O2), which reduced BDNF and phosphorylated CREB and AKT (p-CREB, p-AKT) in a dose-dependent manner. Notably, pretreatment with N-acetylcysteine (NAC) reversed these decreases in a dose-dependent manner. These findings suggest that chronic exercise can ameliorate repeated stress-induced cognitive impairment by detoxifying reactive oxygen species (ROS) in the hippocampus and activating BDNF signaling.
authors.affiliation: Department of Sports and Leisure, Sungshin Women's University, Dongseon 3-ga, Seoungbuk-Gu, Seoul 136-742, South Korea.
authors.forename: Dong-Ho
authors.initials: DH
authors.lastname: Kwon
authors.forename: Bum-Soo
authors.initials: BS
authors.lastname: Kim
authors.forename: Hyukki
authors.initials: H
authors.lastname: Chang
authors.forename: Young-In
authors.initials: YI
authors.lastname: Kim
authors.forename: Sangmee Ahn
authors.initials: SA
authors.lastname: Jo
authors.forename: Yea-Hyun
authors.initials: YH
authors.lastname: Leem
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism*; D003071:Cognition / Q000187:drug effects / Q000502:physiology*; D003072:Cognition Disorders / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D003345:Corticosterone / Q000097:blood; D004305:Dose-Response Relationship, Drug; D005080:Exercise Test / Q000379:methods; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007150:Immunohistochemistry; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018782:Maze Learning / Q000187:drug effects / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D018384:Oxidative Stress; D010766:Phosphorylation; D010805:Physical Conditioning, Animal; D061251:Primary Cell Culture; D017382:Reactive Oxygen Species / Q000378:metabolism; D012149:Restraint, Physical / Q000379:methods; D015398:Signal Transduction; D013315:Stress, Psychological / Q000378:metabolism / Q000473:pathology*
chemical_list: D000447:Aldehydes; D019208:Brain-Derived Neurotrophic Factor; D017382:Reactive Oxygen Species; D008315:Malondialdehyde; D006861:Hydrogen Peroxide; C027576:4-hydroxy-2-nonenal; D003345:Corticosterone; D000111:Acetylcysteine