Expression Of S100A6in Rat Brain Tissues After Traumatic Brain Injury

Traumatic brain injury is the most commonly disease among all kinds of traumaticinjuries, and commonly merge with other various trauma. The high rate of death anddisorder made it the top place of trauma. Consciousness disorder, mild cognitiveimpairment etc. can be seen in the mild TBI patients. While coma, paralysis, seriouscognitive disorder, epilepsy and other nervous system symptoms often appears in thesevere TBI, and serious influence patient survival and quality of life. The hot point ofpathophysiology after TBI focuses on the common pathway lead by all kinds of damagefactors. That is cell necrosis lead by intracellular calcium ion outbreak. With thedevelopment of research on TBI, people became realized that apoptosis also exist. Thenthe mechanism of TBI apoptosis induced by calcium outbreak has become a newresearch direction. The biochemical changes in the nerve cell after TBI still notthoroughly understood. So there has no breakthrough progress about the clinical efficacyof patients with treatment time, method. Apoptosis caused by the combination of scholarsfrom calcium after the outbreak and downstream molecules and anti-apoptotic pathwaysstudies deeply. Studies have found that calcium binding protein S100family can becombined with calcium ion, and can be further combined with further signal transductionwith calcyclin binding protein CacyBp. Thus a cell signal transduction pathway mayexist in the regulation of apoptosis: Ca2+/S100/CacyBp/β-catenin（β-tubulin）. Therehas no report about relationship between cognition function and S100A6changes. Wedesigned the experiment that is to find the S100A6protein changes rule lies in the brainof rat after TBI.Objective To explore the mechanism of nerve damage following traumatic braininjury. Moderate brain injury rat model was built to determine the S100A6protein afterTBI. And to analyze the relationship between TBI and S100A6changes. Aim at theexpression of molecular mechanism of the development of neural cell injury after TBI,and provide valuable theoretical basis and novel points of intervention to improveclinical curative effect. Methods Healthy Seventy-two male SD rats (weight220±20g) were dividedrandomly into TBI group (n=64) and normal control group (n=8). The TBI model wascreated by using lateral head rotation device and subdivided into1h,3h,6h,12h,24h,72h,7d and14d group (8rats per group). The rats were sacrificed and formaldehydeperfusion fixation at each time point. Collection of the brain and tissue paraffin section,then immunochemical method was used to detect the distribution of S100A6protein inthe cortex and hippocampus in rat brain. The expression of the brown stained particleswas considered as "positive" and lack of the stained particles as "negative". Brain slicesin each time point at high magnification images were calculated by image processingsoftware as gray rate expressed by mean±standard deviation. Using U test at the time ofinjury group and the control group were performed two independent sample mean,P<0.05had significant difference.Results Immunohistochemical results showed that S100A6was distributed onnucleus envelope, cytoplasm and cell membrane both in the hippocampus and the cortex.The nuclear envelope, hippocampus and cerebral cortex neuron cells of normal controlgroup showed brown staining in cytoplasm and nuclear membrane. The expression ofS100A6was decreased to the lowest level in the rat brain at1h post TBI (P <0.05) withthe performance of slightly brown staining, then became stronger gradually andrecovered to normal at day7, with no statistical difference compared with normal controlgroup (P>0.05).Conclusion Hippocampus, cortex of S100A6protein decreased to the lowest levelimmediately after TBI. With the time flow the expression of S100A6recovered gradually.And showed no statistically difference at7day group which compared with normal group.It is inferred that S100A6protein binding to the target protein CacyBp with the largenumber of outbreaks of Ca2+at TBI, Caused the decrease shown in immunohistochemicalstaining slices. Then with the start of the cell apoptosis and anti-apoptosis mechanism,the restore of the Ca2+outbreak, and the new synthesis of S100A6protein, the expressionshows recovery. The regular pattern of firstly decreased and then recovered wascoordinated with the regular pattern of clinical patient’s consciousness deep and recoveryand cognitive decline and then rise regularity, Suggested that the injury and recovery hassome relation with the changes of S100A6protein after TBI, not only provide basis forthe further research of cell signal transduction after TBI, but also provide newintervention sites for clinical treatment and shows new ideas for further research.