• Yichao Jin, Yingying Lin, Jun-feng Feng, Feng Jia, Guoyi Gao, and Ji-yao Jiang.
• Department of Neurosurgery, Ren-Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
• World Neurosurg. 2015 Aug 1;84(2):420-30.

ObjectiveMultiple mechanisms participated in the cell death after fluid percussion traumatic brain injury (TBI). In the present study, we evaluated the effect on cell death in the injured cortex after fluid percussion TBI and investigated a possible role of autophagy.MethodsTBI model was induced by a fluid percussion TBI device. Moderate hypothermia (32°C) was achieved by partial immersion in a water bath (0°C) under general anesthesia for 4 hours. All rats were killed at 6 or 24 hours after TBI.ResultsCleaved caspase 3 evaluated with Western blotting and terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate-biotin nick end labeling-positive cells in injured cortex were significantly increased 6 hours after fluid percussion TBI and were further up-regulated 24 hours after TBI, dramatic up-regulation of Beclin-1 and protein light chain-3 expression levels was also observed. Further up-regulation of biomarkers of autophagy, attenuation of caspase 3 up-regulation and reduction of cell death was observed after 4 hours of hypothermia. Immunofluorescence analysis for cell localization demonstrated that protein light chain-3- and Beclin-1-positive cells included neurons and glial cells in the injured cortex after TBI and hypothermic treatment. By ultrastructural observation, autolysosomes in injured cortex were significantly increased at 6 and 24 hours after TBI and were further up-regulated after TBI hypothermic treatment.ConclusionsThese data suggest that hypothermic treatment could attenuate TBI-induced cell death in this fluid percussion TBI model, possibly through activation of autophagy pathway.Copyright © 2015 Elsevier Inc. All rights reserved.

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