Effects Of Sodium Aescinate On Bcl-2 Expression And Neurons Apoptosis In Rats After Traumatic Brain Injury

Traumatic Brain Injury (TBI) are common diseases of neurosurgery It serious impact on human survival and quality of life. After acute brain injury, the neurons can be divided into two forms, One called primary neuronal damage, and the other known as the delayed neuronal injury. Bcause the Primary traumatic injury always occurred at the same time, Secondary injury after trauma-induced neuronal apoptosis has attracted extensive attention. The detection of effects of sodium aescinate on Bcl-2 expression and neurons apoptosis in Rats after Traumatic Brain Injury made a meaningful help to the therapy and research after TBI.Objective: To explore effects of sodium aescinate on Bcl-2 expression and neurons apoptosis in Rats after Traumatic Brain Injury. For the purpose of providing the experiment basis for the further use of sodium aescinate in clinical therapy in traumatic brain injury.Methods: 125 adult maleness Sprague-Dawley (SD) rats were distributed randomly to 4 groups: sham-operated group,model group,saline and sodium aescinate group. The rats in saline and sodium aescinate group were made into brain injury model in the way of fluid percussion brain injury with a pressure of 200kPa. After thd traumatic model of production, Aescin a dose of 5mg/kg/time, concentration of 1mg/mL, at the same time to combat drug delivery methods to be administered by intraperitoneal injection, followed by injection of a frequency of 1/24h. saline group use the same dose and delivery method as the aescin group.Then brains of rats were collected at different time (12h,24h,36h,72h,1w) and were fixed, embedded and sliced, then we determined the change of Bcl-2 expression and neurons apoptosis in tissues,samples of frontal cortex and CA1 district in cornu- ammonis by immunohistochemistry. All datas were observed by IPP image analytical system, then analysised statistically with variance analysis and q test.Results:1. Pathological changeDifferent degree damage in different areas of brain were seen in each group. Some of neurocytes in cortex and hippocampus change into arch form. And lots of akaryocytes diffuse in brain tissue. More necrosis neurocytes emerged in the brain cortex of injury side. Fewer neurocytes were seen in hippocampus. No evident change in normal control group and sham control group.2. Change of Bcl-2 expression2.1 Sham-operated group proto-oncogene Bcl-2 expression negative, Appeared the Bcl-2 appears 12 hours after TBI in Saline group and model group, get a 48-hour peak, then begin to decline. But the odium aescinate group get a 36-hour peak, Early appearance of the product of peak,It aslo made a wider and stronger feature.2.2 The expression of Bcl-2 in model group were significant higher than that in sham-operated group.and had statistically significant differences (P<0.05). Sodium aescinate group were significant higher than that in saline, and had statistically significant differences (P<0.05).3. Change of cell apoptosis3.1 Sham-operated group found only a small amount of apoptosis cells, model group and saline group appears 24 hours after TBI, get a 24-hour peak, then begin to decline.Reinforcement of p38 immunocompetence emerged at the time of 24h after TBI, evident enhancement appeared 3 days later, the peak were reached at the time of 1w and the descent came after 2 weeks. The number of apoptotic cells aescin group was significantly lower than the corresponding control group.3.2 Compare to the other three groups,Sham-operated group had statistically significant differences (P<0.05), there is apoptosis nerve cells in rats after TBI. Aescin treatment group stained TUNEL-positive cells after 24 hours less than the model group with the saline control group, and had statistically significant differences (P<0.05).and it get much higher than sham-operated group. and had statistically significant differences (P<0.05). Conclusions:1. Diffuse hemorrhage and neurocyte necrosis were seen at the areas beyond injury part after TBI.2. The expression of Bcl-2 enhance evidently in the areas of cortex and hippocampus CA1.3. There are a lot of apoptosis cell in the areas of cortex and hippocampus CA1.4. Sodium aescinate increases Bcl-2 protein expression in rats after traumatic buain injury and make a earlier peak.5. After TBI in rats, Aescin could inhibit neuronal apoptosis by increasing the Bcl-2 protein expression.