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目的:探讨新生豚鼠胆红素脑神经损伤元时脑源性神经营养因子(BDNF)及受体酪氨酸激酶B(TrKB)在大脑皮质及海马表达特点。方法:取生后2～5天内的豚鼠60只,随机分为3组,C组、T1组、T2组。C组为对照组;T1组:腹腔注射晶体胆红素100μg/g;T2组腹腔注射胆红素200μg/g,分别在4h、8h处死。做脑组织切片,电镜,光镜观察病理改变,并采用免疫组化和图像分析,观察不同时间点BDNF、TrKB在皮层及海马表达变化。结果:①胆红素脑神经元损伤模型成功建立。②T14h、T24h在早期皮层及海马是降低的。随时间延长,BDNF表达明显上升,T14h、T24h与C4h比较,P<0.05,T14h、T24h与T18h、T28h比较,P<0.05。③TrKB在皮层和海马表达是随时间延长和损伤加重表达增加,T14h、T18h、T24h、T28h与C4h、C8h比较,P<0.05。结论:胆红素脑神经元损伤中,皮层和海马BDNF、TrKB升高可能减轻神经元损伤,在抑制神经元凋亡和神经元修复中发挥重要作用,有利神经元修复和再生,可能是胆红素脑神经元损伤时机体的自我保护机制之一。
Objective: To investigate the expression of brain-derived neurotrophic factor (BDNF) and receptor tyrosine kinase B (TrKB) in cerebral cortex and hippocampus of neonatal guinea pig during bilirubin neuronal injury. Methods: Sixty guinea pigs within 2 to 5 days after birth were randomly divided into 3 groups: C group, T1 group and T2 group. Group C was the control group. T1 group: intraperitoneal injection of crystalline bilirubin 100μg / g; T2 group bilirubin 200μg / g intraperitoneal injection, were killed at 4h, 8h. The brain tissue sections, electron microscope and light microscope were used to observe the pathological changes. Immunohistochemistry and image analysis were used to observe the expression of BDNF and TrKB in cortex and hippocampus at different time points. Results: ① Bilirubin neuronal injury model was successfully established. ② T14h, T24h in the early cortex and hippocampus is reduced. Compared with C4h at T14h, T24h and C4h, P <0.05, T14h, T24h and T18h, T28h, P <0.05. (3) The expression of TrKB in cortex and hippocampus increased with time and injury, P <0.05 compared with C4h and C8h in T14h, T18h, T24h, T28h and C4h, C8h. CONCLUSION: Elevated BDNF and TrKB in cortical and hippocampal neurons during bilirubin neuronal injury may reduce neuronal damage, play an important role in inhibiting neuronal apoptosis and neuronal repair, favoring neuronal repair and regeneration, which may be the gall bladder One of the mechanisms of the body’s self-protection during the injury of neurons of the red blood cells.