2002Clinical neurosurgeryRequires access

Inhibitory Effects of Mild Hypothermia on Posttraumatic Neuronal Apoptosis in Rats

Tan Haibin

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Abstract

Objective To study the mechanisms of posttraumatic neuronal apoptosis and the protective effect of mild hypothermia on posttraumatic brain in the rats. Methods By using the terminal deoxynucletidyl transferase -mediated deoxyuridine 5'-triphosphate-biotin nick end labeling technique (TUNEL), agarose gel electrophoresis and flow cytometric analysis, the dynamic change in the processes of neuronal apoptosis in the different brain regions of the rats subjected to severe traumatic brain injury (TBI) were sequentially examined. The animals were randomly divided into three groups:①sham;② rats with head injury, killed at 12, 24, 48, 72, 168, 336 hours after TBI;③ rats with head injury, treated by mild hypothermia at 32t for 6, 12 and 24 hours respectively. Results The apoptotic cells could be detectable in the cerebral cortex, subcortex, white matter and the hippocampus 12 h~14 d after TBI and reached the peak at approximately 12~72 h. The apoptotic cells in the above-mentioned brain areas significantly increased in the rats with brain injury compared with the control group (P0.05). Agarose gel electrophoresis showed specific apoptotic zone, and a typical DNA ladder could be revealed by the flow cytometric analysis in the rats with brain injury. In the rats with brain injury treated by mild hypothermia, the apoptotic cells were significantly fewer than those in the rats with brain injury who were not treated by the mild hypothermia (P0.05). Conclusions The data suggest that apoptosis would occur after TBI. The mild hypothermia may exert favorable effect on inhibition of apoptotic cell death.

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Objective To study the mechanisms of posttraumatic neuronal apoptosis and the protective effect of mild hypothermia on posttraumatic brain in the rats. Methods By using the terminal deoxynucletidyl transferase -mediated deoxyuridine 5'-triphosphate-biotin nick end labeling technique (TUNEL), agarose gel electrophoresis and flow cytometric analysis, the dynamic change in the processes of neuronal apoptosis in the different brain regions of the rats subjected to severe traumatic brain injury (TBI) were sequentially examined. The animals were randomly divided into three groups:①sham;② rats with head injury, killed at 12, 24, 48, 72, 168, 336 hours after TBI;③ rats with head injury, treated by mild hypothermia at 32t for 6, 12 and 24 hours respectively. Results The apoptotic cells could be detectable in the cerebral cortex, subcortex, white matter and the hippocampus 12 h~14 d after TBI and reached the peak at approximately 12~72 h. The apoptotic cells in the above-mentioned brain areas significantly increased in the rats with brain injury compared with the control group (P0.05). Agarose gel electrophoresis showed specific apoptotic zone, and a typical DNA ladder could be revealed by the flow cytometric analysis in the rats with brain injury. In the rats with brain injury treated by mild hypothermia, the apoptotic cells were significantly fewer than those in the rats with brain injury who were not treated by the mild hypothermia (P0.05). Conclusions The data suggest that apoptosis would occur after TBI. The mild hypothermia may exert favorable effect on inhibition of apoptotic cell death.

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Available abstract

Objective To study the mechanisms of posttraumatic neuronal apoptosis and the protective effect of mild hypothermia on posttraumatic brain in the rats. Methods By using the terminal deoxynucletidyl transferase -mediated deoxyuridine 5'-triphosphate-biotin nick end labeling technique (TUNEL), agarose gel electrophoresis and flow cytometric analysis, the dynamic change in the processes of neuronal apoptosis in the different brain regions of the rats subjected to severe traumatic brain injury (TBI) were sequentially examined. The animals were randomly divided into three groups:①sham;② rats with head injury, killed at 12, 24, 48, 72, 168, 336 hours after TBI;③ rats with head injury, treated by mild hypothermia at 32t for 6, 12 and 24 hours respectively. Results The apoptotic cells could be detectable in the cerebral cortex, subcortex, white matter and the hippocampus 12 h~14 d after TBI and reached the peak at approximately 12~72 h. The apoptotic cells in the above-mentioned brain areas significantly increased in the rats with brain injury compared with the control group (P0.05). Agarose gel electrophoresis showed specific apoptotic zone, and a typical DNA ladder could be revealed by the flow cytometric analysis in the rats with brain injury. In the rats with brain injury treated by mild hypothermia, the apoptotic cells were significantly fewer than those in the rats with brain injury who were not treated by the mild hypothermia (P0.05). Conclusions The data suggest that apoptosis would occur after TBI. The mild hypothermia may exert favorable effect on inhibition of apoptotic cell death.

Key concepts: Apoptosis, TUNEL assay, Medicine, Hypothermia, Traumatic brain injury, Hippocampus, Agarose gel electrophoresis, Anesthesia

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