| Objective:To observe the pathological changes of brain tissue, and measure the expression of Bcl-2, Bax and apoptosis rate at different time points in each group,to explore the influence of NGF on expression of Bcl-2 and Bax in brain tissue after hyperbilirubinemia in neonatal rats.Methods:90 7-day-old SD rats were randomly divided into three groups(n=30 each group):A group(control group), B group(hyperbilirubinemia model group) and C group(hyperbilirubinemia + NGF intervention group), each group were divided into five sub-groups(n=6 each)based on different time points after hyperbilirubinemia(6, 12, 24,48, and 72 hours), the animals were euthanized and harvested for brain tissues at different points. Using hematoxylin and eosin staining to observe the pathological changes of brain tissue in each group, and the apoptosis rate of nerve cells was measured by TUNEL method.Expressions of Bcl-2 and Bax were detected with immunohistochemistry.Results:(1)Compared with the control group, the apoptosis of nerve cell in the hippocampus of the model group was increased(F 值=278.862,P=0.000﹤0.05), the expression of Bcl-2 increased(F 值=203.556,P=0.000﹤0.05), the expression of Bax increased significantly(F 值=139.163,P=0.000﹤0.05), the difference was statistically significant(P < 0.05).(2)Compared with the model group, after NGF intervention, the expression of Bcl-2 was significantly increased(F 值=44.448,P=0.000﹤0.05), the expression of Bax decreased significantly(F 值=12.574,P=0.001﹤0.05), and the apoptosis rate of nerve cells in hippocampus was decreased(F 值=30.289,P=0.000﹤0.05), but the expression of Bax and apoptosis rate were higher than those in control group(P < 0.05).Conclusion:(1)Bcl-2 and Bax may participated in neuronal apoptosis in hyperbilirubinemia of neonatal rats;(2)NGF may play a protective role in the brain by up regulating the expression of Bcl-2, down regulating the expression of Bax and inhibiting neuronal apoptosis in hippocampus. |
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