BACKGROUND: Body cooling (BC) or mild hypothermia therapy (about 33°C) is reportedly effective for spinal cord injury (SCI). However, the mechanisms underlying the beneficial effects of BC remain unclear, so does BC ameliorating SCI via promoting neurogenesis, anti-inflammation, and angiogenesis. METHODS: The standard rat compression SCI model was tested hypothetically in two groups: one receiving BC (33°C) and the other, normothermia (37°C). Afterward, the effects of BC therapy on the hind limb locomotion, spinal cord infarction and apoptosis, angiogenesis, neurogenesis, and inflammation in these two groups of SCI were assessed. The other group of sham SCI was used as controls. RESULTS: Apoptosis (evidenced by higher numbers of terminal deoxynucleotidyl- transferase-mediated and duDP-biotin nick end-labeling-positive cells), infarct, activated inflammation (evidenced by higher levels of tumor necrosis factor-α, interleukin-1β, and myeloperoxidase), and hind limb locomotor dysfunction were inspected in the untreated (37°C) SCI rats 4 days after SCI. When compared with those of untreated SCI rats, SCI rats receiving BC (33°C) displayed lower levels of apoptosis, infarct volume, activated inflammation, and hind limb locomotor dysfunction. In addition, that BC promoted both angiogenesis (evidenced by increased numbers of both vascular endothelial growth factors and bromodeoxyuridine-positive endothelial cells) and neurogenesis (evidenced by increased numbers of both glial cell line-derived neurotrophic growth factors and bromodeoxyuridine-neuronal-specific nuclear protein double positive cells) in the injured spinal cord was evaluated 4 days after SCI. CONCLUSION: BC (33°C) improved SCI outcomes by promoting angiogenesis, neurogenesis, and anti-inflammation in a rat SCI model.
BACKGROUND: Body cooling (BC) or mild hypothermia therapy (about 33°C) is reportedly effective for spinal cord injury (SCI). However, the mechanisms underlying the beneficial effects of BC remain unclear, so does BC ameliorating SCI via promoting neurogenesis, anti-inflammation, and angiogenesis. METHODS: The standard rat compression SCI model was tested hypothetically in two groups: one receiving BC (33°C) and the other, normothermia (37°C). Afterward, the effects of BC therapy on the hind limb locomotion, spinal cord infarction and apoptosis, angiogenesis, neurogenesis, and inflammation in these two groups of SCI were assessed. The other group of sham SCI was used as controls. RESULTS: Apoptosis (evidenced by higher numbers of terminal deoxynucleotidyl- transferase-mediated and duDP-biotin nick end-labeling-positive cells), infarct, activated inflammation (evidenced by higher levels of tumor necrosis factor-α, interleukin-1β, and myeloperoxidase), and hind limb locomotor dysfunction were inspected in the untreated (37°C) SCI rats 4 days after SCI. When compared with those of untreated SCI rats, SCI rats receiving BC (33°C) displayed lower levels of apoptosis, infarct volume, activated inflammation, and hind limb locomotor dysfunction. In addition, that BC promoted both angiogenesis (evidenced by increased numbers of both vascular endothelial growth factors and bromodeoxyuridine-positive endothelial cells) and neurogenesis (evidenced by increased numbers of both glial cell line-derived neurotrophic growth factors and bromodeoxyuridine-neuronal-specific nuclear protein double positive cells) in the injured spinal cord was evaluated 4 days after SCI. CONCLUSION:BC (33°C) improved SCI outcomes by promoting angiogenesis, neurogenesis, and anti-inflammation in a rat SCI model.
Authors: Anil Maybhate; Charles Hu; Faith A Bazley; Qilu Yu; Nitish V Thakor; Candace L Kerr; Angelo H All Journal: Crit Care Med Date: 2012-02 Impact factor: 7.598