| Hypoxic-ischemic encephalopathy (HIE)of newborn is aninjury disease of nervous system, which is caused by differenthypoxic-ischemic (HI) factors in perinatal period and shows highmortality rate. HIE is common reason to result in nervous systeminvalid of children and become investigative focus. Therefore,peoplealways want to search one kind of way for therathy in HIE and lessenof it,s sequel. NGF is relation to the survival, immigration, growthand differentiation of nerve cells , and simultaneously has theconnection with others,cell functionality.When hypoxiaischemic brain damage happened in neonate,endogenous NGF always increases. Because disposition of NGF hasselectivity and its quantity is limit,it makes therapy of exogenousNGF become impossible. Means of Exogenous NGF therapy diseaseof central nervous system included NGF infused into brain issues bylateral cerebral ventricle, explantating NGF producing cell intodamage neurocyte, gene therapy et al.Because these means hadweakness such as immaturity, specification and paradamage,they weredifficultily developed in clinical. So deeply study the expression andprotective mechanism is very impossible and meaningful.NGF is hydrosoluble protein molecule, so more exidence abouttherapy of NGF on HIE is deficient.Thus in this study we made themodel of neonate HIBD rats by normal pressure hypoxia cabin, andcompare normal groups , HIBD groups and NGF therapy groups bythe mean of immunohistochemistry and pathology. We observe thechange of rats` weight growth, brain tissue moisture capacity, cellapoptosis, synaptophysin, and reach the conclusion which NGF havethe proactive effection in neonate rats with hypoxic brain damaged.This will supply the evidence for therapy of HIE.ObjectiveTo explore protective effection of Exogenous Nerve GrowthFactor in neonate rats with Hypoxic-Ischemic Brain Damaged.MethodsSixty of 7days olds healthy postnatal Wistar rats with body massof 11-18g,half males and half females,were provided by theExperimental Center of baxic medical college. Forty rats are madeinto HIBD models and all rats were divided into three groups, whichis normal groups , HIBD groups and NGF therapy groups. After HIthirty minutes,NGF therapy groups were injected β-NGF by themeans of intraperitoneal injection,and it would keep on three times.But saline was injected into other groups in the same time and way.All rats were put to death and picked up specimens after 72 hours.Then, we determine the change of each group rats` weight growth,brain tissue moisture capacity. Some HBID models rats were perfusedwith an aldehyde fixative. Their brain tissues were fixed, embeddedand sliced, then we determined the change of cell apoptosis andsynaptophysin in tissues,samples of frontal cortex and CA1 district incornu ammonis by immunohistochemistry and pathology. All dataswere observed by IPP image analytical system ,then analysisedstatistically with variance analysis and q test.Results:1.By the comparison with each group rats` weight growth,wemade the conlusion as follows:Firstly HIBD groups and Normalcontrol groups had statistically significant differences(P<0.05).Secongly weight growth of NGF therapy groups andNormal control groups had not statistically significant differences(P>0.05), that were higher HIBD groups, and had statisticallysignificant differences(P<0.05).2.By the comparison with each group rats` brain tissue moisturecapacity,we made the conlusion as follows:Firstly HIBD groups andNormal control groups had statistically significant differences(P<0.05).Secongly brain tissue moisture capacity of NGF therapygroups and Normal control groups had not statistically significantdifferences(P>0.05), that were lower HIBD groups, and hadstatistically significant differences(P<0.05).3. Through light microscope p38 positive reactant showed browngranula in endochylema. It represented by correct optical densityvalue(COD). In the study we found p38 positive reactant in frontalcortex and CA1 district in cornu ammonis of HIBD groups was higherthan normal control groups . It showed that the synaptophysin ofneonate HI rats was reduced. NGF therapy groups was lower thanHIBD groups.,and they had statistically significant differences(P<0.05). It showed after damage happened in central nerve system,NGF had regulating effection in the process of regeneration andrecovery.4. The positive apoptosis cell character was cell bodydiminution,karyopycnosis, nuclear fragmentation and apoptotic bodyby the dyeing of TUNEL. We compared the different groups withodds ratio of positive apoptosis cells and all cells in the same samplein field of 400 vision. In this study there were many positive apoptosiscells in frontal cortex and CA1 district in cornu ammonis of HIBDgroups, and through light microscope it had brown cell nucleus. NGFtherapy groups was lower than HIBD groups,and had statisticallysignificant differences(P<0.05). Then it higher than normal controlgroups, and had statistically significant differences(P<0.05).Conclusion:1. After therapy of NGF in HBID rats body weight was obviouslyincreased, thus NGF could relieve the HIBD clinical symptom.2. After therapy of NGF in HBID rats brain edema lessened. Itcould delay occurrence of brain edema and lighten the extent of brainedema.3. After therapy of NGF in HBID rats synaptophysin in neonaterat brain increased, and it showed NGF produced a marked effect inCNS regeneration and reparation.4. After therapy of NGF in HBID rats apoptosis cell in neonaterat brain reduced, and it showed NGF could lingten apoptosis andbrain damage.5. NGF by periphery had the protective effection forhypoxia-ischemia brain damage of neonatal Wistar rats.In a word,when neonatal rats happened in hypoxiaischemia braindamage,NGF can get through the blood brain barrier,then it willlessen the brain edema,lingten cell apoptosis or cell necrosis andpromote synapse regeneration. This kind of mechanism can protectbrain damage. This study will provide theoretical basic and appliedpossibility. It will open up a new way for the effective therapy of HIEpatients.
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