Exercise inhibits neuronal apoptosis and improves cerebral function following rat traumatic brain injury

被引:70
作者
Itoh, Tatsuki [1 ]
Imano, Motohiro [2 ]
Nishida, Shozo [3 ]
Tsubaki, Masahiro [3 ]
Hashimoto, Shigeo [4 ]
Ito, Akihiko [1 ]
Satou, Takao [1 ,5 ,6 ]
机构
[1] Kinki Univ, Sch Med, Dept Pathol, Osaka 5898511, Japan
[2] Kinki Univ, Sch Med, Dept Surg, Osaka 5898511, Japan
[3] Kinki Univ, Sch Pharmaceut Sci, Osaka 5898511, Japan
[4] PL Hosp, Div Pathol, Osaka, Japan
[5] Kinki Univ Hosp, Sch Med, Div Hosp Pathol, Osaka, Japan
[6] Kinki Univ, Inst Life Sci, Div Sports Med, Osaka 5898511, Japan
关键词
Cerebral dysfunction; Neuroprotection; Apoptotic cell death; Neuronal degeneration; CENTRAL-NERVOUS-SYSTEM; CELL-DEATH; GROWTH-FACTOR; ISCHEMIA; ACTIVATION; PROTECTS; MICE; NEUROPROTECTION; HIPPOCAMPUS; RECEPTOR;
D O I
10.1007/s00702-011-0629-2
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Exercise is reported to inhibit neuronal apoptotic cell death in the hippocampus and improve learning and memory. However, the effect of exercise on inhibition of neuronal apoptosis surrounding the area of damage after traumatic brain injury (TBI) and the improvement of cerebral dysfunction following TBI are unknown. Here, we investigate the effect of exercise on morphology and cerebral function following TBI in rats. Wistar rats received TBI by a pneumatic controlled injury device were randomly divided into two groups: (1) non-exercise group and (2) exercise group. The exercise group ran on a treadmill for 30 min/day at 22 m/min for seven consecutive days. Immunohistochemical and behavioral studies were performed following TBI. The number of single-stranded DNA (ssDNA)-positive cells around the damaged area early after TBI was significantly reduced in the exercise group compared with the non-exercise group (P < 0.05). Furthermore, most ssDNA-positive cells in the non-exercise group co-localized with neuronal cells. However, in the exercise group, a few ssDNA-positive cells co-localized with neurons. In addition, there was a significant increase in neuronal cell number and improvement in cerebral dysfunction after TBI in the exercise group compared with the non-exercise group (P < 0.05). These results indicate that exercise following TBI inhibits neuronal degeneration and apoptotic cell death around the damaged area, which results in improvement of cerebral dysfunction. In summary, treadmill running improved cerebral dysfunction following TBI, indicating its potential as an effective clinical therapy. Therefore, exercise therapy (rehabilitation) in the early phase following TBI is important for recuperation from cerebral dysfunction.
引用
收藏
页码:1263 / 1272
页数:10
相关论文
共 46 条
[1]   Impaired mitochondrial function, oxidative stress and altered antioxidant enzyme activities following traumatic spinal cord injury [J].
Azbill, RD ;
Mu, XJ ;
BruceKeller, AJ ;
Mattson, MP ;
Springer, JE .
BRAIN RESEARCH, 1997, 765 (02) :283-290
[2]   Exercise Increases Neural Stem Cell Number in a Growth Hormone-Dependent Manner, Augmenting the Regenerative Response in Aged Mice [J].
Blackmore, Daniel G. ;
Golmohammadi, Mohammad G. ;
Large, Beatrice ;
Waters, Michael J. ;
Rietze, Rodney L. .
STEM CELLS, 2009, 27 (08) :2044-2052
[3]   Effect of a neuroprotective exercise protocol on oxidative state and BDNF levels in the rat hippocampus [J].
Cechetti, Fernanda ;
Fochesatto, Cintia ;
Scopel, Denise ;
Nardin, Patricia ;
Goncalves, Carlos Alberto ;
Netto, Carlos Alexandre ;
Siqueira, Ionara Rodrigues .
BRAIN RESEARCH, 2008, 1188 :182-188
[4]   Forced, moderate-intensity treadmill exercise suppresses apoptosis by increasing the level of NGF and stimulating phosphatidylinositol 3-kinase signaling in the hippocampus of induced aging rats [J].
Chae, Chang-Hun ;
Kim, Hyun-Tae .
NEUROCHEMISTRY INTERNATIONAL, 2009, 55 (04) :208-213
[5]  
CHAN PH, 1985, PROG BRAIN RES, V63, P227
[6]   Traumatic brain injury induced cell proliferation in the adult mammalian central nervous system [J].
Chirumamilla, S ;
Sun, D ;
Bullock, MR ;
Colello, RJ .
JOURNAL OF NEUROTRAUMA, 2002, 19 (06) :693-703
[7]   Oxygen free radical-dependent activation of extracellular signal-regulated kinase mediates apoptosis-like cell death after traumatic brain injury [J].
Clausen, F ;
Lundqvist, H ;
Ekmark, S ;
Lewén, A ;
Ebendal, T ;
Hillered, L .
JOURNAL OF NEUROTRAUMA, 2004, 21 (09) :1168-1182
[8]  
Dressler Jan, 2009, Leg Med (Tokyo), V11 Suppl 1, pS54, DOI 10.1016/j.legalmed.2009.02.024
[9]   CENTRAL NERVOUS-SYSTEM TRAUMA AND STROKE .2. PHYSIOLOGICAL AND PHARMACOLOGICAL EVIDENCE FOR INVOLVEMENT OF OXYGEN RADICALS AND LIPID-PEROXIDATION [J].
HALL, ED ;
BRAUGHLER, JM .
FREE RADICAL BIOLOGY AND MEDICINE, 1989, 6 (03) :303-313
[10]   Targeted disruption of the bcl-2 gene in mice exacerbates focal ischemic brain injury [J].
Hata, R ;
Gillardon, F ;
Michaelidis, TM ;
Hossmann, KA .
METABOLIC BRAIN DISEASE, 1999, 14 (02) :117-124