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

Abstract

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.

miR21 is Associated with the Cognitive Improvement Following Voluntary Running Wheel Exercise in TBI Mice

“…It is suggested that spontaneous exercise may be therapeutic in the management of CNS injury, by reducing the degree of initiatory damage, limiting the degree of secondary neuronal death, improving neuronal plasticity and cognitive function, stabilizing rhythmic firing patterns of spinal motoneurons, promoting recovery and neural repair (Griesbach Tao Hu, Feng-Jie Zhou and Ye-Fei Chang contributed equally to this work. et al 2009;Itoh et al 2011). It is well demonstrated that practice of physical exercise increased adult hippocampal neurogenesis and enhances behavioral performance in rodents; however, the possible mechanisms underlying are still not well known (VanLeeuwen et al 2010).…”

Effects of Voluntary Physical Exercise, Citicoline, and Combined Treatment on Object Recognition Memory, Neurogenesis, and Neuroprotection after Traumatic Brain Injury in Rats

“…42 There are also a few reports that physical exercise applied after brain damage may reduce neuron loss and inflammatory responses. For example, both forced and physical exercise reduced neuron loss after TBI, 9,43,44 and after hippocampal domoic acid damage. 45 Piao et al 14 have also reported neuroprotective effects of voluntary physical exercise after TBI in mice.…”

“…[7][8][9] Some evidence suggest that it can also confer benefits in humans. 10 These benefits seem to be mediated by a variety of mechanisms such as increased angiogenesis, cell proliferation and neurogenesis, enhanced synaptic plasticity, and regulation of inflammatory responses.…”

“…9,14 This is of outstanding importance, given the chronic nature of most TBI sequels and the feasibility of physical exercise as a long-term treatment in humans.…”

“…10 These benefits seem to be mediated by a variety of mechanisms such as increased angiogenesis, cell proliferation and neurogenesis, enhanced synaptic plasticity, and regulation of inflammatory responses. 9,[11][12][13][14][15] Thus, physical exercise seems to be a promising tool in promoting functional recovery after TBI.…”