The Research Of Rat Hippocampus TDP-43and PGRN Protein Expression After Traumatic Brain Injury

Objectives:Through the TDP-43and PGRN protein expression after acute traumatic brain injury, we can explore the relationship between head trauma and neurodegenerative diseases, and hope to provide appropriate guidelines for head trauma early prevention of neurodegenerative diseases.Methods:Healthy Sprauge-Dawley rats which weight from220to270grams and similar months of age (2-3months),were divided randomly into two group:the normal control group and the TBI model group.And each group was divided randomly into five subgroups:these rats were allowed to survive for1day,3days,7days,14days and28days. All rats in experimental groups had suffered from Traumatic brain injury after free-fall, The rats of TBI model group suffered head impact injury, and the normal control group suffered the same impact and preparation before the surgery, but not be injured. Keep in the same environment conditions of rearing, to be put to death and extract the brain tissue in five different time points.Then use immunohistochemical staining of TDP-43and PGRN protein expression in hippocampus neurons and HE staining of rat brain tissue pathological changes in cell morphology.Results:1. From the first day, the TDP-43protein content in Rat hippocampal tissue neurons cytoplasmic TDP-43protein of TBI model group gradually increased, reached a peak in the7days,and gradually decline in28days basically reach the same level as the normal control group. Still slightly higher than the normal level. The cytoplasm TDP-43positive protein expression in the TBI model group were significantly higher than normal control group at the each same point (P<0.05).2.The PGRN protein expression in hippocampus neurons of TBI model group was opposite with the TDP-43protein.PGRN protein within neurons gradually decreased from day1to7days,to reach their peak in the7days, and then gradually return to normal, close to the normal level in the first28days. Microglia around neurons were activated and hyperplasia in the post-traumatic, PGRN protein surrounding glial cells gradually increased, reached a peak in7days, and then gradually reduced, with the repair of neurons, basically the same as normal control group in28days. The TBI model group at each time point neurons of PGRN (nPGRN)-positive protein expression were higher than the same period the normal control group (P<0.05); TBI model of hippocampus tissue in the microglia the PGRN (mPGRN) positive protein expression higher than the same period the normal control group (P<0.05).Conclusions:After acute brain trauma, rat hippocampus neurons pathological TDP-43increased first and then decreased, in the28days, close to the normal level, but there is a small amount of pathological TDP-43residual in a small part of rats; neurons PGRN first decreased and then increased, surrounding glial cells PGRN first increased and then decreased, close to the normal in28days, small amount of residual gum PGRN can also be found in some rats.