Traumatic Brain Injury Exposed In Low-temperature Environment, Nerve Cells Apoptosis And Apoptosis Protein Bcl-2,Bax Changes

Purpose To investigate the changes of nerve cell apoptosis and apoptosis protein Bcl-2,Bax in rats after traumatic brain injury(TBI) in low-temperature environment.Methods Eighty healthy SD rats(body weigh 250~350g ) were randomly divided into common temperature control group,low-temperature control group,common temperature trauma group and low-temperature trauma group. Improved Feeney's free falling body epidural strike method was used to cause traumatic brain injury, rats of low-temperature trauma group were put into low-temperature environment for 4h after trauma, then fed in 25℃room temperature, rats of common temperature trauma group were fed in 25℃room temperature after trauma, rats of common temperature control group were given the same treament as common temperature control group except trauma, rats of low-temperature control group were given the same treament as low-temperature trauma group except trauma; body temperature of rats in each group was measured before, 2h and 4h after trauma respectively. Rats in each group were decapitated and brain samples were collected d1,d3,d5,d7 after trauma,brain tissue water content was calculaed, HE dying and TUNUL kit was used to detect cell aptosis in brain tissue , immunohistochemisty was used to measure the expreesion of Bcl-2,Bax. Positive cell counts in high power field were calculated under microscope and difference of positive cell count percentage were compared.Results There was no significant changes in body temperature before and after injury in Common temperature control group,low-temperature control group and common temperature trauma group; low-temperature trauma group's body temperature gradually decreased after exposed in low temperature environment. Brain tissue water content of common temperature trauma group and low-temperature trauma group were significantly increased after injury, but the two groups was no significant statistical difference compared to its time. The apoptosis positive cells were significantly increased after injury in common temperature trauma group and low-temperature trauma group, d3 peak, then gradually decreased in both groups, compared to the same time there is significant statistical difference(P <0.05). The apoptotic protein Bcl-2, Bax expression increased after injury in common temperature trauma group and low-temperature trauma group, but the two paragraphs of the Bcl-2 also showed no statistical difference, while the low-temperature trauma group was significantly higher than common temperature trauma group of Bax expression(P <0.05).Conclusion Low-temperature environment can cause significant changes of body temperature in rats after TBI, and promote neuronal apoptosis Bax protein expression,then promote neuronal apoptosis. Inhibition of Bax expression in low-temperature environment is conducive to reduce apoptosis in brain injury that has the potential value to improve efficacy of treatment.