Treadmill exercise inhibits traumatic brain injury-induced hippocampal apoptosis.
Traumatic brain injury (TBI) occurs when an outside force impacts the brain. The main problem associated with TBI is neuronal cell death of the brain, and the outcome of TBI ranges from complete recovery to permanent disability, and sometimes death. Physical exercise is known to ameliorate neurologic impairment induced by various brain insults. In the present study, we investigated the effects of treadmill exercise on short-term memory and apoptosis in the hippocampus following TBI in rats. TBI was induced by an electromagnetic-controlled cortical impact. The rats in the exercise group were forced to run on a treadmill for 30min once daily for 10 consecutive days, beginning 2days after induction of TBI. For the current study, a step-down avoidance task, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, Western blot for Bcl-2 and Bax, and immunohistochemistry for caspase-3 were conducted. The present results revealed that TBI impaired short-term memory, and increased DNA fragmentation and caspase-3 expression in the hippocampus. Induction of TBI also enhanced expression of pro-apoptotic factor Bax protein and suppressed expression of anti-apoptotic factor Bcl-2 protein in the hippocampus. Treadmill exercise alleviated short-term memory impairment, and decreased DNA fragmentation and caspase-3 expression in the hippocampus. In addition, treadmill exercise remarkably suppressed expression of Bax protein and slightly increased expression of Bcl-2 protein in TBI-induced rats. The present study showed that treadmill exercise might overcome TBI-induced apoptotic neuronal cell death, thus facilitating recovery following TBI.
Kim
Dong-Hyun
DH
Department of Physiology, College of Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.
Ko
Il-Gyu
IG
Kim
Bo-Kyun
BK
Kim
Tae-Woon
TW
Kim
Sung-Eun
SE
Shin
Mal-Soon
MS
Kim
Chang-Ju
CJ
Kim
Hong
H
Kim
Kyeong-Mi
KM
Baek
Seung-Soo
SS
D000704:Analysis of Variance; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001362:Avoidance Learning / Q000502:physiology; D015153:Blotting, Western; D001930:Brain Injuries / Q000378:metabolism / Q000503:physiopathology*; D053148:Caspase 3 / Q000378:metabolism; D002540:Cerebral Cortex / Q000293:injuries*; D003345:Corticosterone / Q000097:blood; D053938:DNA Fragmentation; D006624:Hippocampus / Q000378:metabolism / Q000503:physiopathology*; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008297:Male; D008570:Memory, Short-Term / Q000502:physiology; D009474:Neurons / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000502:physiology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D051028:bcl-2-Associated X Protein / Q000378:metabolism
D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D053148:Caspase 3; D003345:Corticosterone