| Objective: Neonatal hypoxic-ischemic encephalopathy (hypoxic-ischemicencephalopathy, HIE) is caused by perinatal asphyxia partial or complete lack of oxygen,cerebral blood flow caused by reduction or suspension of fetal or neonatal brain injury,there is no effective treatment. The establishment of neonatal SD rats with hypoxicischemic encephalopathy (hypoxic-ischemic brain damage, HIBD) model, givenrecombinant human erythropoietin (recombinant human erythropoietin, rh-EPO)intervention groups at different time points observed large pathological changes of braintissue detected in peripheral blood of each group at different time points interleukin-1β(interleukin-1β, IL-1β) levels of erythropoietin in neonatal SD rat HIBD inflammatoryresponse.Methods: The new7day old SD rats, either sex, weighing12~16g,90were randomlydivided into3groups, HIBD model group, rh-EPO treatment group and sham group.Preparation of Modified Rice HIBD model, HIBD group (n=30) in the model ofnormal saline immediately after preparation of0.5ml/only; rh-EPO treatment group (n=30) in the model were injected intraperitoneally immediately after preparation ofrh-EPO4000U/kg/only, rh-EPO was diluted to0.5ml; sham operation group (n=30)only free but not ligated left common carotid artery, no hypoxia; based on observationof behavioral indicators of the behavior observed in each group; false surgery group,HIBD model group and rh-EPO treatment group were6h,12h,24h,48h,72h each timepoint,6rats, decapitated, the left brain and the blood, hematoxylin-eosin staining(hematoxylin-eosin staining, HE) staining, observed under the microscope in braintissue pathological changes. ELISA assay IL-1β levels in blood, and finally using SPSS17.0statistical software for statistical processing.Results:⑴HIBD neonatal SD rats after different degrees of abnormal behavior.⑵HE staining:①sham operation group at different time points were normal brain sizeand shape, structure clear, closely aligned neurons.②ischemia and hypoxia6h: clearlayer cortical neurons, the cell gap increases, neuronal cell shrinkage deformation.Ischemia and hypoxia12h: level of cortical neurons more clear space between cellsincreases markedly, vacuolar degeneration of nerve cells, nuclear stained. After hypoxia-ischemia24h: disordered cortical neurons, the cell gap increases further,showing that neurons deformation, shrinkage, nuclear stained cells decreased in normalneurons, a significant expansion of cortical capillaries, within the lumen more red bloodcell aggregation. Ischemia and hypoxia48h: disordered cortical neurons, the cell gapwas significantly increased neuronal cell deformation, shrinkage, stained normalneurons was significantly reduced, a significant expansion of capillaries, perivascularcompartment expanded, in red blood cells leak into the compartment. Ischemia andhypoxia72h: unclear level of cortical neurons, the cell gap was significantly increasedneuronal cell deformation, shrinkage, stained to further reduce the normal neurons, asignificant expansion of the capillary around the vessels to further expand the lacunarshows a large necrotic lesions.③rh-EPO treatment group: rh-EPO treatment6h: clearlayer cortical neurons, the cell gap increases, neuronal cell deformation, damage HIBDgroup than the corresponding light. rh-EPO treatment12h: level of cortical neurons isrelatively clear, the cell gap was increased, neuronal cell degeneration, injury HIBDgroup than the corresponding light. rh-EPO treatment24h: disordered cortical neurons,the cell gap to further increase neuronal cell deformation, shrinkage, nuclear stainedcells decreased in normal neurons, injury HIBD group than the corresponding light.rh-EPO treatment48h: disordered cortical neurons, the cell gap was significantlyincreased neuronal cell deformation, shrinkage, nuclear stained cells of normal neuronswas significantly reduced injury group compared with the corresponding light HIBD.rh-EPO treatment72h: unclear level of cortical neurons, the cell gap was significantlyincreased neuronal cell deformation, shrinkage, stained to further reduce the normalneurons, showing necrosis, injury group compared with the corresponding light HIBD.⑶IL-1β results: HIBD model group, rh-EPO treatment group compared with the shamgroup, SD rats at all time points in peripheral blood of IL-1β levels were increased (P<0.01, statistically significant difference), and show their own variation of the shamgroup, rh-EPO treatment group and HIBD group values of serum IL-1βOD were in6h:0.40±0.059;0.45±0.072;0.50±0.044;12h, respectively:0.38±0.037;0.58±0.031;0.70±0.032;24h, respectively:0.40±0.031;0.49±0.042;0.52±0.029;48h,respectively:0.40±0.030;0.48±0.034;0.51±0.034;72h, respectively:0.39±0.030;0.46±0.028;0.48±0.024; HIBD IL-1β in rats6h and12h in the peripheral blood ofIL-1β levels were significantly increased, and the upward trend,24h to reach peak, butstill high72h; rh-EPO HIBD treatment group and model group, serum IL-1β content was significantly (P <0.05), at each time point of serum IL-1β levels decreasedcorrespondingly.Conclusion:⑴rh-EPO on neonatal rats HIBD intervention can significantly reducethe pathological changes in brain tissue, suggesting that rh-EPO on neonatal rat HIBDhave neuroprotective effects.⑵rh-EPO treatment significantly reduced peripheralblood of neonatal rats after HIBD inflammatory factors IL-1β release, which may berh-EPO to play a neuroprotective role in one of the mechanisms. |
PDF Full Text Request