Expression of Antiapoptotic Survivin and Aven Genes in Rat Heart Tissue After Traumatic Brain Injury

We have recently shown that experimental traumatic brain injury (TBI) results in ultrastructural damage in heart tissue. The aim of this study was to determine the two antiapoptotic signals “survivin” and “aven” in rat heart tissue following TBI, and comparing the effects of erythropoietin (EPO) and methylprednisolone (MPS). Thirty-six Wistar-Albino female rats weighing 190 to 230 g were randomly allocated into six groups: group 1 underwent head trauma with no treatment; group 2 and group 3, head trauma and intraperitoneally delivered EPO (1000 IU/kg) and MPS (30 mg/kg), respectively; group 4 (vehicle), head trauma and intraperitoneal albumin (0.4 mL/rat); groups 5 and 6, control and sham-operated groups, respectively. Three-hundred g-cm impact trauma was produced by the method of weight-drop. Real-time quantitative polymerase chain reactions were used to estimate survivin and aven gene expression at the total RNA level. Both survivin and aven were higher among the treatment than the trauma group (P = .0006, .0001 and P = .0038, .0033, respectively). Comparing survivin and aven between EPO and MPS treatment groups showed no significance (P = .3027, .2171, respectively). Also, both survivin and aven were significantly higher among the treatment than the vehicle, the control, or the sham-operated groups. These findings suggested that both EPO and MPS may play important roles in the expression of antiapoptotic survivin and aven genes in heart tissue after TBI.