| Background Traumatic brain injury is the most common disease neurological disease of injury. It has a serious threat to human life. Their disability morbidity and mortality rates is high and have upward trend every year. Our large population base population grew faster, regardless of illness or the onset of the number are staggering. Earlier reports indicated 10 million people worldwide occur traumatic brain injury each year, which has 5.8 million people died due to brain injury, accounted for 10% of the world's population died. According to forecasts to 2020 year TBI will become the world's third largest category of disease. In the study of traumatic brain injury, the mainly focused on the clinical aspects, such as traumatic brain injury treatment, prognosis, and other aspects of rehabilitation, Traumatic brain injury first aid, advantages and disadvantages of various treatment modalities, cognitive disorders after treatment care, after-effects, etc. However, research on endogenous protective mechanism of traumatic brain injury is relatively small. Brain damage caused by brain trauma mainly direct damage and indirect secondary brain injury, direct or indirect cause of neuronal apoptosis and traumatic brain edema caused by secondary damage. The brain is an important organ tissues of animals and humans, Including a large number of neurons in the cerebral cortex, is an important regional control action, language, thinking activity. Scientists has found in humans and animals experimental. Traumatic brain injury after cerebral cortex can cause serious behavioral, language impairment, mental activity, severely affected the patient's condition and prognosis. There is currently no effective treatment and protection measures, especially endogenous protective mechanism. Therefore, the study of the brain's protective mechanisms after traumatic brain injury and the measures of international and domestic hot research topic in recent years. After brain injury, the nerve cells release glutamate mainly excitatory neurotransmitter, Activation of glutamate receptors and directly or indirectly start voltage-dependent Ca2+ channels. A large number Ca2+ influx makes intracellular Ca2+ overload. Ca2 + and calcium regulatory proteins combined, further reaction and makes the role of cortical neurons is compromised. On the other hand,a large amount of superoxide anion generation, further reaction of peroxynitrite ion or nitrite ions, thereby further inhibiting energy metabolism. Inhibition of energy metabolism and free radical damage to the cells lining the increase, resulting in swelling of mitochondria in cells caused by many factors such as apoptosis. In recent years, we have found in the study of traumatic brain injury in the brain and also releases large amounts of glutamate release a peptide neurotransmitt glutamate N-acetylaspartate a neuroprotective effect. NAAG to glutamate release after the trauma has a strong inhibitory effect. NAAG peptidase located on glial cells, However, soon after the release of NAAG peptidase NAAG hydrolysis into N-acetyl aspartate and glutamate,So lost neuroprotection. Whereby NAAG peptidase activity is inhibited,Thereby inhibiting the degradation of NAAG. Increasing the concentration of NAAG's synaptic cleft,reducing further damage of glutamate release in the pathological process. NAAG peptidase inhibitors have been successfully synthesized in a large number of experiments,and further confirmed its protective effect in glutamate toxicity model of excessive release of glutamate. However inhibitor vulnerable environment and other aspects such as their drug concentration, affect its stability,NAAG peptidase gene can be more stable eliminate expression of NAAG peptidase after excluding, thus play a neuroprotective effect. At present, research at the genetic level is rare fresh.Part? Influence of mice GCP? gene knockout on neurons after traumatic brain injuryObjective To study changes of apoptosis neuron around the neuron injury area and nerve function between C57BL/6J mice and GCP?gene knockout mice after traumatic brain injury.Methods A total of 20 male GCP?gene knockout mice and 20 male wild-type C57BL/6J mice were used in this experiment. Gene knockout mice were randomly divided into two groups(KO + TBI group, n=10; KO +sham TBI group, n=10), and wild-type C57BL/6J mice were randomly divided into two groups(WT + TBI group, n=10; WT + sham TBI group, n=10). TBI model was made by CCI. Set the parameter(impact velocity 1.5m/s, reaching depth 1.0mm, remained in the brain for 80ms). 24 h after TBI making neural function score, immunofluorescence staining, neuron apoptosis counting around the brain injury area.Results Our results showed that GCP? gene knockout mice administration improved neural function score and protected neuron around the brain injury area after 24 h following TBI(P <0.05).Conclusion Our findings suggest that GCP ? gene knockout exert its protective effect on brain by reducing neuron apoptosis.Part ? Influence of mice GCP?gene knockout on brain edema after traumatic brain injuryObjective To study cerebral edema changes between C57BL/6J mice and GCP? gene knockout mice and to investigate the relationship between GCPII gene knock out and cerebral edema after TBI.Methods A total of 20 male GCP II gene knock out mice and 20 C57BL/6J mates were used in this experiment. Gene knockout mice were randomly divided into two groups(KO + TBI group, n=10; KO +sham TBI group, n=10), and C57BL/6J mates were randomly divided into two groups(WT+ TBI group, n=110; WT + sham TBI group, n=10).Moderate TBI model was made by CCI. Set the parameter(impact velocity 1.5m/s; reaching depth 1.0mm;remained in the brain for 80ms)?The rotarod test, brain water content, edema volume and signal intensity ratio of T2 WI in the injury area were evaluated at 24 h after TBI.Results Our results showed that GCP?gene knockout mice administration improved neurological deficits after 24 h following TBI(p < 0.05). GCP ?gene knockout reduced brain water content, edema volume and signal intensity ratio of T2 WI in the injury brain area(p < 0.05).Conclusion Our findings suggest that GCP ? gene knockout exert its protective effect on brain by reducing cerebral edema after TBI. |
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