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Effects Of Glutamic-oxalacetic Transaminase On Cerebral Edema And Neurological Function After Traumatic Brain Injury In Rats

Posted on:2022-04-04Degree:MasterType:Thesis
Country:ChinaCandidate:S F ZhouFull Text:PDF
GTID:2494306509996779Subject:Master of Clinical Medicine
Abstract/Summary:PDF Full Text Request
BackgroundTraumatic brain injury(TBI)poses a serious threat to human life and quality of life.TBI includes primary craniocerebral injury and secondary craniocerebral injury,the latter aggravates neurological impairment through inflammatory response,glutamate(Glu)toxicity and calcium overload,etc.Therefore,it is of great significance to improve secondary craniocerebral injury after TBI.Glutamate Oxaloacetate Transaminase(GOT)accelerates the clearance of Glutamate in the brain by increasing the concentration gradient of Glutamate across the blood-brain barrier and alleviates brain injury.At present,there are few reports on the effect of GOT on secondary craniocerebral injury in patients with TBI.ObjectiveThe closed craniocerebral injury model in SD rats was established to verify whether GOT could inhibit the inflammatory response and alleviate the neurological damage after brain edema,so as to improve the secondary craniocerebral injury after TBI.Methods1.A total of 126 SD rats were selected and divided into normal group(Sham group),traumatic brain injury group(TBI group)and GOT treatment group(TBI+GOT group),with 90 rats in group A(n=30)and 36 rats in group B(n=12).2.The experimental animal model was made according to Feeney DM method,and0.9%Na Cl was given to Sham group and TBI group.In TBI+GOT group,GOT was subcutaneously injected into the neck(0.3mg/kg,once /1d)after modeling.3.The neurological deficit of rats after modeling was evaluated by the modified neurological deficit score(m NSS).4.Wet and dry weight method was used to detect the water content in the damaged lesion and surrounding brain tissue.5.He staining was used to observe the morphological changes of brain tissue cells around the lesion.6.Enzyme-linked immunosorbent assay(ELISA)was used to determine the expression of inflammatory cytokines TNF-α and IL-6 in the lesion and surrounding brain tissues.7.The expression of inflammatory cytokines TNF-α and IL-6 was detected by immunofluorescence technique.8.Statistical Methods: SPSS21.0 statistical software was used to analyze the data.Results1.m NSS score: The score of Sham group was 0-2,while the score of TBI group and TBI+GOT group was >2,which reached the highest score 12 h after modeling.Compared with TBI group,TBI+GOT score decreased(P<0.05).2.The content of water in the injured and surrounding brain tissues was significantly higher in TBI group and TBI+GOT group than in Sham group(P<0.05),and the peak value was(82.05±1.15)% at 3d after modeling;Compared with TBI group,water content in TBI+GOT group decreased(P<0.05).3.HE staining: cells in the Sham group were regular in morphology and orderly in arrangement,with clear blue staining of nuclei,normal blood vessels,and no inflammatory cell infiltration.In the TBI group,the cell body was swollen,the space was enlarged,some nucleoli were wrinkled and thickened,blood vessels were dilated,and inflammatory cell infiltration was visible.In TBI+GOT group,the number of cell swelling was less and the degree was less,the space was smaller,the number of nucleolar shrinkage was less,vascular dilatation was rarely seen,and a small amount of inflammatory cell infiltration was found.4.ELISA method: Compared with Sham group,the expression of TNF-α and IL-6 in TBI group was significantly increased(65.60±9.84 and 83.03±9.24)(P<0.05);Compared with the TBI group,the expression of TNF-α and IL-6 in the TBI+GOT group decreased to50.52±7.13 and 65.73±10.65(P<0.05).5.Immunofluorescence staining showed that TNF-α and IL-6 were more expressed in TBI group than in Sham group.The fluorescence expression of TNF-α and IL-6 decreased significantly in TBI+GOT group compared with TBI group.ConclusionGOT can reduce the expression of inflammatory factors TNF-α and IL-6,reduce brain edema and neurological function injury,and thus improve the secondary craniocerebral injury after TBI.
Keywords/Search Tags:Traumatic Brain Injury, Glutamate oxaloacetate transaminase, The inflammatory response, Nerve protection
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