Effect of Recombinant Human Erythropoietin on Zinc-Induced Traumatic Brain Injury in Rats

Traumatic Brain Injury (TBI) is one cause of neuronal death that results in losing memory, anxiety, and depression. Researches indicate that zinc contributes to transmission in synapses in the central nervous system(CNS) but is released in toxic level from neurons in TBI synaptically. Releasing zinc from the presynaptic neuron in TBI aggravates inflammation in brain. The aim of this study is assessing the effectof Recombinant Human Erythropoietin (RhEpo) on neuronal survival after TBI. In this present case-control study, 30 male Sprague-Dawley rats with weight 250- 300 gr were divided into three groups: RhEpo, control, and sham. Hippocampal neurons of rats in control andRhEpo groups were cultured and exposure to 200μM ZnCl2 in 20 minutes. This procedure caused neuronal injury that was revealed by observing nerve morphology. Mitochondrial function measurement showed that 24 hours before zinc exposure, using RhEpo resulted in aremarkable increase of neuron survival in RhEpo group (0.6007) vs in the control group (0.2333, p<0.01). Also study showed that application of RhEpo 30 minutes after TBI stopped neuronal death which was revealed by ZP2, a zinc-specific fluorescent sensor to show neuronaldamage. However mechanism of RhEpo function in TBI is not clear, data’s show a significant effect of RhEpoon decreasing neuronal death (p<0.01). These results demonstrate RhEpo can dramatically reduce Zn2+ releasing in the hippocampus after TBI. Understandingoptimal RhEpo and zinc serum level in persons with TBI can help to treatment strategies.