| Objective:to perinatal asphyxia in neonates with hypoxic ischemic encephalopathy (hypoxic,ischemicencephalopathy, HIE) the fatality rate and the remaining sequelae of very highprobability, a severe threat to the quality of life of newborns. The main reason is: the centralnervous impairment after regeneration ability, only symptomatic treatment can alleviate thesymptoms, also cannot reduce the possibility of the bequeath sequela. The old idea ofregeneration after central nervous system injury is very difficult, but recent research showsthat: the central nervous internal environment in the presence of the inhibition of nerveregeneration factor, seriously affecting the central neural regeneration. According to thepresent domestic and foreign research, it is not difficult to find the common central nervousinhibitory factor are the following: Nogo-A, myelin associated glycoprotein(myelin-associated glycoprotein, MAG) and oligodendrocyte myelin glycoprotein (aoligodendrocyte-myelin glycoprotein, OMgp), English name is Neurite outgrowth Nogo-Ainhibitor–A, it is a kind of human being RTN4gene coding for the protein, is thought to becentral nervous system neurite growth inhibitors. These inhibitory factor common inhibitorynerve cell regeneration, they pass through the same receptor (Nogo receptor, NgR) play arole, and Nogo-A on the inhibition of damaged neural function is more intense.The animal experimental study aimed to further explore the treatment of neonatalhypoxic ischemic encephalopathy. Using immunohistochemical method, HE staining in thedetection of neonatal rat brain with the number of Nogo-A positive cells and observation ofneonatal rat brain tissue pathological situations; give newborn rat gangliosides (GM1),close observation of the periods of time each brain tissue, the number of Nogo-A positivecells and nerve cell growth situation, explore Nogo-A in neonatal rat HIBD brain injury inrats, observation of GM1on rat Nogo-A inhibition of brain cell regeneration effect and whether it can be protected by hypoxia and ischemia caused by injury to nerve cells.Methods:907day-old rats were randomly divided into three groups: control group, HIBD groupand GM1group.①the control group (n=30): only free left common carotid artery, ligation,not hypoxia, given by intraperitoneal injection of saline0.25ml/kg.②HIBD group (salinegroup)(n=30): preparation of HIBD model immediately after intraperitoneal injection ofsaline0.25ml/kg. As the group for3days, the GM1treatment group (n=30): preparation ofHIBD model immediately after intraperitoneal injection of GM-120mg/kg/days, afterintraperitoneal injection of diluted to0.5ml. Visual grouping situation for3days. All groupswere12h,24h, and72h three point in time to collect specimens,10rats in each group. Eachanimal were treated to12h,24h,72h when the decapitation death. The brain tissue sampleswere soaked in30%sucrose,40g/L paraformaldehyde solution, for3days, using paraffinfixed, sectioned, through HE staining was observed in the cerebral tissue of neonatal ratwith pathological conditions; by immunohistochemical method to observe the number ofNogo-A positive cells.Results:by immunohistochemical method was observed in the control group3slots on thecerebral tissue of neonatal rat with the number of Nogo-A positive cells along with the agegrowth and increased slightly; group HIBD: Nogo-A positive cells in the model24isincreased, to72hours is still slightly higher trend; group GM1: Nogo-A the number ofpositive cells of early increased gradually, to24h number, then started to decrease, theapplication of GM1, after hypoxia ischemia Nogo-A positive cell number was increased by.Through HE staining:①12h time points were observed: neurons showed edema, localneurons appear disappears,②pyknosis in24h time point observation: neurons oedema, adecrease in the number, disappears, and nuclear pyknosis; nerve stromal edema.③72h timepoints were observed in neurons of cerebral cortex: the decrease of the number, loss ofnormal structure, astrocyte swelling, cerebral parenchymal necrosis, proliferation of glialcells.Conclusion:Nogo-A in hypoxic ischemic brain damage after the number of positive cells increasedsignificantly, inhibition of CNS regeneration after injury, the ganglioside GMl in hypoxicischemic brain damage after partial inhibition of Nogo-A expression, a stabilization of cellmembrane, reduce cell edema. |
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