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Effect Of Hypoxia Preconditioning On The Changes Of HIF-1α And VEGF In The Brain Tissue In Rats With Traumatic Brain Injury

Posted on:2015-01-04Degree:MasterType:Thesis
Country:ChinaCandidate:L ZhangFull Text:PDF
GTID:2254330431957853Subject:Surgery
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Background In modern military plateau warfare,Will face significant non-combatattrition caused by acute high altitude reaction,Coupled with hypoxic-ischemic braininjury is undoubtedly the "worse".How protective effects of altitude hypoxia harshenvironments, Plateau has become the main focus of military medicalresearch.Traumatic brain injury after brain ischemia and hypoxia are the main factorsleading to brain damage.Hypoxic preconditioning in advance to give the body a shorttime irritant hypoxia, Subsequent severe ischemia, anoxia significant defensecapability,it is the current anti-hypoxia/ischemia research focus.hypoxia-induciblefactor-1α is the main factor regulating oxygen concentration-dependent,On thesurrounding environment with a strong sensitivity to oxygen.VEGF is HIF-1αdownstream encoded target proteins,it can be involved in nerve vascular remodelingto achieve neuroprotection.Through the establishment of rat model of traumatic braininjury,to study in rats after traumatic brain contusion surrounding brain tissue HIF-1αand VEGF expression,and observe hypoxia preconditioning on both.Objective (1)Through the establishment of rat model of traumatic brain injury,Contusion surrounding brain tissue HIF-1α and VEGF expression was observed aftertraumatic brain injury in rats;(2) Through the establishment of hypoxicpreconditioning model,Observe the effects of hypoxic preconditioning in rat brainafter traumatic brain contusion surrounding HIF-1α and VEGF expression in theprevention and treatment of hypoxic preconditioning on hypoxic-ischemic brain damage provide a theoretical basis.Method204Sprague-Dawley rat (male) were randomly divided into controlgroup(Con n=12), traumatic brain injury group(TBI n=96)and Hypoxicpreconditioning group(HPC n=96). TBI group was established rat model oftraumatic brain injury by adopting improved Feeney free fall, Weight50g weightsfrom rat bone window surface height25cm whereabouts blow, HPC group of ratswere placed in a hypobaric chamber for hypoxic preconditioning (50.47kPa,3d,3h/d),brain damage caused by the same method. The control group did not receive brainblow. After injury1h,4h,8h,12h, and1d,3d,7d,14d time points decapitated. ByRT-PCR, Western blotting and immunohistochemical staining method to detect thesurrounding brain tissue contusion foci HIF-1α, VEGF expression, doubleimmunofluorescence assay VEGF distribution and coexistence case, and performstatistics analysis.Result①After craniocerebral injury,4rat died in group TBI,1died in groupHPC, a total of5, new model.Difficulty in breathing after injury in rats,Immediatelygiven to maintain airway patency and cardiac massage,Rat vital signs graduallyreturned to normal after recovery.After injury in rats awake at about4-5h, poor stateafter you wake up, not eating.Follow-rat epilepsy4, paralysis of limbs2.TBI groupafter injury3days of not eating rats were killed3, give again model, finally entered theanalysis of results of experimental rats204only.②Contusion surrounding brain tissueafter traumatic brain injury in rats HIF-1α were significantly increased after injury4,8,12h and1,3d(P<0.05).HIF-1α mRNA peaked at12h, protein peaked at1d,Hypoxic preconditioning group of HIF-1α expression gradually increases1h afterinjury,HIF-1α mRNA and protein were more significantly upregulated in4h~7d(P<0.05),until after the injury14d expression tend to be norma(lP>0.05).Contusionsurrounding brain tissue after traumatic brain injury in rats VEGF were significantlyincreased after injury4h,VEGF mRNA expression peaked after injury1d, protein reached a peak3d,until injury7d(P<0.05).Hypoxic preconditioning group ofVEGF expression gradually increases1h after injury,HIF-1α mRNA and protein weremore significantly upregulated in4h~7d(P<0.05).There was no statistical differencebetween the groups in14d(P>0.05).③Double immunofluorescence assay hypoxicpreconditioning group after injury3d VEGF expression was significantly more thantraumatic brain injury group, which can be positioned on VEGF expression neurons,glial cells and vascular endothelium.Conclusion①Weight50g weight from rat bone window surface25cm heightwhereabouts fight can be made stable traumatic brain injury model in rats, stability isbetter.②Contusion surrounding brain tissue after traumatic brain injury in ratsHIF-1αand VEGF over time showed a crest-like change,Tip traumatic brain injury inbrain tissue ischemia and hypoxia-inducible expression of HIF-1α,and modulatesdownstream target VEGF proteins involved in nerve system protection.③Hypoxicpreconditioning can be pre-activated HIF-1α expression of brain tissue,to enhance theVEGF increases. This may be the prevention of hypoxic-ischemic brain injurymechanisms of brain tissue damage.
Keywords/Search Tags:hypoxic preconditioning, traumatic brain injury, HIF-1α, VEGF, rat, brain tissue
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