Effect of hypothermia on apoptosis in traumatic brain injury and hemorrhagic shock model |
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| Affiliation: | 1. Kırıkkale University, Faculty of Medicine, Department of Emergency Medicine, Kırıkkale, Turkey;2. Kırıkkale University, Faculty of Medicine, Medical Biochemistry, Kırıkkale, Turkey;3. Kırıkkale University, Faculty of Medicine, Pathology, Kırıkkale, Turkey;4. Kırıkkale University, Faculty of Medicine, Department of General Surgery, Kırıkkale, Turkey;1. Exeter Hip Unit, Princess Elizabeth Orthopaedic Centre, Royal Devon and Exeter NHS Foundation Trust, Barrack Road, Exeter, EX2 5DW UK;2. Orthopaedic Research Unit, Institute of Health and Biomedical Innovation, Queensland University of Technology, The Prince Charles Hospital, Chermside, Queensland, 4037 Australia;1. Department of Oral and Maxillofacial Surgery/Pathology & 3D Innovation Lab, VU University Medical Center/Academic Centre for Dentistry Amsterdam (ACTA), Amsterdam, The Netherlands;2. Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, University of Hasanuddin, Makassar, Indonesia;3. Department of Oral and Maxillofacial Surgery, University of Oulu, Oulu University Hospital, Oulu, Finland;1. Trauma Research Unit Department of Surgery, Erasmus MC, University Medical Center Rotterdam, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands;2. Department of Anatomy and Neurosciences, Erasmus MC, Rotterdam, The Netherlands |
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| Abstract: | IntroductionThe neuroprotective mechanisms of therapeutic hypothermia against trauma-related injury have not been fully understood yet. In this study, we aimed to investigate the effects of therapeutic hypothermia on biochemical and histopathological markers of apoptosis using Traumatic brain injury (TBI) and hemorrhagic shock (HS) model.MethodsA total of 50 male albino-wistar rats were divided into five groups: Group isolated TBI, Group NT (HT + HS + normothermia), Group MH (HT + HS + mild hypothermia), Group MoH (HT + HS + moderate hypothermia) and Group C (control). Neurological deficit scores were assessed at baseline and at 24 h. The rats were, then, sacrificed to collect serum and brain tissue samples. Levels of Caspase-3,6,8, proteoglycan-4 (PG-4), malondialdehyde (MDA), and nitric oxide (NO) were measured in serum and brain tissue samples. Histopathological examination was performed in brain tissue.ResultsThere were significant differences in the serum levels of Caspase-3 between Group NT and Group C (p = 0.018). The serum levels of Caspase-6 in Group NT (0.70 ± 0.58) were lower than Group MH (1.39 ± 0.28), although the difference was not statistically significant (p = 0.068). There were significant differences in the brain tissue samples for Caspase-3 levels between Group NT and Group C (p = 0.049). A significant difference in the Caspase-8 brain tissue levels was also observed between Group NT and Group C (p = 0.022). Group NT had significantly higher scores of all the pathological variables (for edema p < 0.017; for gliosis p < 0.001; for congestion p < 0.003, for hemorrhage p < 0.011) than Group C.ConclusionOur study results suggest that hypothermia may exert its neuroprotective effects by reducing markers of apoptotic pathway, particularly Caspase-3 on TBI and HS. |
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| Keywords: | Animal study Caspase Experimental Hemorrhagic shock Traumatic brain injury Hypothermia Proteoglycan-4 |
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