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目的探讨神经生长因子干预对高胆红素血症新生大鼠脑组织Bcl-2和Bax表达的影响。方法选择7日龄SD新生大鼠90只,随机分为3组:对照组30例,高胆红素血症模型组30例,神经生长因子干预组30例,各组根据处死时间不同又分为6 h、12 h、24 h、48 h和72 h 5个亚组,每个亚组6只。各组在各时间点取脑组织,用苏木素-伊红染色法观察各组脑组织病理改变,脱氧核糖核苷酸末端转移酶介导的缺口末端标记法测定脑组织细胞凋亡率,免疫组织化学法测定Bcl-2和Bax表达。结果 1与对照组相比,模型组海马区神经细胞凋亡增加,Bcl-2表达轻度升高,Bax表达明显升高,差异有统计学意义(P<0.05);2与模型组比较,NGF干预后,Bcl-2表达明显升高(P<0.05),Bax蛋白表达明显降低(P<0.05),海马区神经细胞凋亡减少(P<0.05),但Bax表达和凋亡率仍高于对照组(P<0.05)。结论 1Bcl-2和Bax可能参与了新生大鼠高胆红素血症神经细胞凋亡的发生;2NGF可能通过上调Bcl-2表达,下调Bax表达,抑制神经细胞凋亡,从而发挥其脑保护作用。
Objective To investigate the effect of nerve growth factor (NGF) intervention on the expression of Bcl-2 and Bax in brain tissue of neonatal rats with hyperbilirubinemia. Methods Ninety SD neonatal SD rats were randomly divided into three groups: control group (30 cases), hyperbilirubinemia model group (30 cases) and nerve growth factor intervention group (30 cases). Each group was divided according to the time of death 6 subgroups, 6 subgroups at 6 h, 12 h, 24 h, 48 h and 72 h respectively. At each time point, brain tissue was taken from each group, pathological changes of brain tissue were observed by hematoxylin-eosin staining, apoptotic rate of brain tissue was measured by nick-end labeling Bcl-2 and Bax expression was determined chemically. Results Compared with the control group, the apoptosis of hippocampal neurons in model group increased slightly, the expression of Bcl-2 slightly increased and the expression of Bax increased significantly (P <0.05). 2 Compared with the model group, After NGF intervention, Bcl-2 expression was significantly increased (P <0.05), Bax protein expression was significantly decreased (P <0.05), apoptosis of hippocampal neurons was decreased (P <0.05), but Bax expression and apoptosis rate were still high In the control group (P <0.05). Conclusions 1Bcl-2 and Bax may be involved in the neuronal apoptosis of neonatal rats with hyperbilirubinemia. 2NGF may play a neuroprotective role by up-regulating Bcl-2 expression, down-regulating Bax expression and inhibiting neuronal apoptosis .