| Background Both in times of peace or war traumatic brain injury are commontrauma types. It is currently the main focus worldwide military medical research.Contusion area local ischemia, hypoxia and mechanical damage after traumatic braininjury caused by blood-brain barrier (BBB) destroy, resulting in brain tissue injuryedema, cerebral edema and further aggravate ischemic brain tissue hypoxia, creating avicious cycle. To protect the integrity of the blood-brain barrier after traumatic braininjury in order to reduce cerebral edema and improve the prognosis is currently a hotissue of domestic and foreign researches. Claudin-5, a brain endothelial cell tightjunction proteins, is an important part of the BBB. Sphingosine kinase1(SphK-1) is asphingosine1phosphate (Sph) to generate a key enzyme sphingosine1phosphate, andit is an important factor vascular endothelial barrier protection. In recent years, it hasbeen found protective effects of hypoxic preconditioning on nerves, blood vessels inthe area, such as cerebral ischemia, but the exact mechanism has not been fullyelucidated. The topics to be established rat model of traumatic brain injur, and injuryby hypoxia observed after pretreatment with traumatic brain injury caused by twogroups of rats brain tissue Claudin-5, sphingosine kinase1, the blood-brain barrierpermeability and changes in brain water content, and to explore hypoxicpreconditioning on blood-brain barrier permeability after traumatic brain injury andbrain edema.Objective (1) To establish a rat model of traumatic brain injury;(2) To research of Claudin-5,SphK-1experssion and blood-brain barrier permeability changes aftertraumatic brain injury in rats;(3) To research the effect of hypoxic preconditioning ontraumatic brain injury in rat cortical brain tissue Claudin-5, SphK-1expression andpermeability of the blood brain barrier permeabilityMethod (1) using ZH-ZYQ type mechine to made a rat model of traumatic braininjury, a blow to open the site to the midline2mm, herringbone stitch front2mm,50gweight falling from25cm height to combat brain injury caused by moderate toestablish a stable animal model;(2) the use of animal positions and vacuum pumpconnected device consisting of hypobaric hypoxia, low pressure in the closed positionof the animal within the simulated hypobaric hypoxia conditions, the semi drove intothe air inlet to ensure continuous suction air flow caused by the vacuum pump, the sizeof the intake negative pressure openness to regulate air intake, and converted intoaltitude5500m (atmospheric pressure50.47kpa), for3h a day for three days, three dayslater in the same way line freefall brain injury blow.(3) After the rats were injured1h,4h,8h,12h,1d,3d,7d,14d time points cortex killed specimens were detected by usingRT-PCR, Western blotting and immunohistochemical methods tissue expression ofClaudin-5and Sphk1of IgG staining of brain tissue and brain tissue water content.Result (1) TBI group Claudin-5expression after injury1h began lowering,8~12h toa minimum,1d began to rise gradually until14d after injury tends to control group ratsafter hypoxic preconditioning injury Claudin-5TBI group expressed similar trend, buttime points were higher than those TBI group.(2) Rats of TBI group SphK-1expression began to increase after injury1h,1d rose highest,14d to normal levels,hypoxic preconditioning SphK-1expression in rats with traumatic trends were similar,but higher than TBI group (3) IgG score in TBI group reach the highest spot at12hafter TBI until the14d is still higher than the normal control group, HPC group at eachtime point scores were lower than TBI group. Conclusion (1) via a hypobaric chamber with a vacuum pump (50.47kpa,3d,3h/d),can produce a stable model of hypoxic preconditioning.(2) After traumatic brain injury,The expression of Claudin-5and SphK-1in the cerebral cortex tissue into a wavy,closely related to both the blood-brain barrier permeability.(3) Hypoxicpreconditioning can upregulate Claudin-5and SphK-1expression in early traumaticbrain injury, protect the integrity of BBB and reduce Cerebral edema. |
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