Abstract

To study the effects of recombinant human erythropoietin on inflammatory factors in rats with traumatic brain injury is the main objective. A total of 45 specific-pathogen-free grade male Sprague-Dawley rats were randomly assigned into sham operation group (sham group), model group and recombinant human erythropoietin intervention group (treatment group) (n=15). Model and treatment groups were prepared into traumatic brain injury model by hitting the head through the modified Feeney’s free-fall impact method, while the head of sham group was not hit. After modeling, treatment group was intraperitoneally injected with recombinant human erythropoietin at 5000 IU/kg daily and sham and model groups were intraperitoneally injected with the same dose of normal saline. The rats were killed after 7 d of continuous administration. The changes of brain mitochondrial membrane potential were detected through rhodamine 123 staining and immunocytochemistry and Western blotting were separately employed to measure the expressions of interleukin-1β, interleukin-6 and tumor necrosis factor-α in brain tissues and the expression levels of dynamin-related protein 1, fission 1, mitofusin 2 and optic atrophy 1, mitochondrial dynamics related proteins in brain tissues. Compared with sham group, model group exhibited significantly weakened rhodamine 123 fluorescence intensity, increased expressions of interleukin-1β, interleukin-6 and tumor necrosis factor-α, dynamin-related protein 1 and fission 1 and reduced expressions of mitofusin 2 and optic atrophy 1 in brain tissues (p<0.05). In comparison with model group, treatment group had significantly enhanced rhodamine 123 fluorescence intensity, reduced expressions of interleukin-1β, interleukin-6 and tumor necrosis factor-α, dynamin-related protein 1 and fission 1 and elevated expressions of mitofusin 2 and optic atrophy 1 in brain tissues (p<0.05). Recombinant human erythropoietin can protect the brain after traumatic brain injury by relieving the inflammatory response and mitochondrial injury after traumatic brain injury.