Biochemical and Apoptotic Biomarkers of Experimentally Induced Traumatic Brain Injury: In Relation to Time since Death

Abstract

The present study declares the relationship between the cause of death and postmortem biochemical marker alterations in CSF, serum and plasma. In addition, immunohistochemical and microarchitecture examination of brain tissue of White New Zealand rabbits at different PMI after traumatized death. Thirty adult male White New Zealand rabbits were divided into two main equal groups; the first was physically killed by cervical dislocation and the second through head trauma. Each group was subdivided into three PMIs (zero, 6, and 12hrs PM). CSF was used to detect the levels of K+, Na+, Ca++, albumin While, lactic acid, hypoxanthine, ammonia and uric acid concentrations were measured in plasma. Estimation of HMGB1, IL-1β and TNF-α were assessed in serum. In addition to immunohistochemical observations of Bcl-2 and P53 apoptotic proteins in brain tissue. The results revealed that some of the examined parameters as K+, Na+, albumin, ammonia, hypoxanthine and HMGB1 had the potential role in estimation of PMI at examined time periods in physical and traumatized death. Traumatic death induced severe cerebral hemorrhages and necrosis of cerebral parenchyma than physical death. Immunohistochemical results of P53 and Bcl-2 in brain tissue declared focal positive reactions of some neurons, astrocytes and microglia in different degrees with time since death. It was concluded that biochemical analysis of some body fluids, tissue pathological changes and apoptotic markers are applicable tools for assessing accurate PMI after traumatic brain injury and could have a crucial role in legal medicine