TIMING OF TRAUMATIC BRAIN INJURY AND ITS SYSTEMIC EFFECTS ON THE LUNGS OF ADULT MALE ALBINO RATS

Abstract

Objective: Timing of traumatic brain injury (TBI) is very common and important especially, in forensic autopsy cases with no signs of intracranial hemorrhage or contusion and with short time of survival following head injury. In such cases it is difficult to determine the cause of death. TBI results in systemic inflammatory responses that are complicated by dysfunction of peripheral organs such as the lungs, liver and intestine. The lung is especially critical in the setting of lung transplantation, where more than half of donor allografts are obtained postmortem from individuals with TBI. The aim of the present study was to assess post-intervals of traumatic brain injury and to evaluate the effects of TBI on lungs by measuring serum levels of High mobility group box 1 protein (HMGB1), performing quantitative real-time polymerase chain reaction (qPCR) analysis for gene expression and detecting any histopathological changes or immunohistochemical reaction of brain and lungs. Materials and Methods: Fifty four adult male albino rats divided into in to 3 groups (18 rats each): Group I: Negative control: rats left without any intervention. Group II: (sham): rats were anesthetized with ether inhalation and left without TBI inflection. Group III (TBI): rats were anesthetized with ether inhalation then the head was placed on platform and brain injury was done by weight drop method. After TBI infliction, six rats from group III (TBI) at each time point (1 st, 3rd& 7thday) and six rats from group I&II were anesthetized and blood samples were drawn for measuring serum level of (HMGB1).Then rats were sacrificed, specimens from contused cerebral cortex and lungs were subjected to quantitative real-time polymerase chain reaction (qPCR) analysis for gene expression of HMCB1, histopathology examination and immunohistochemical detection of HMGB1 immunoreaction. Results: Traumatic brain injury induced time dependent up-regulation of HMGB1 in serum and qPCR gene expression. Significant histopathological inflammatory changes and positive HMGB1 immunoreaction of brain and lung tissues of TBI (group III) were detected when compared with both control groups. Conclusion: It can be concluded that traumatic brain injury induced time dependent changes in serum and tissue levels of HMGB1, also histopathological changes in the brain and lungs of adult male albino rats. So, this marker can be useful for the diagnosis and timing of brain trauma and predict post TBI lung injury.