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目的探讨新生豚鼠胆红素脑神经损伤时脑源性神经营养因子(BDNF)mRNA及其受体酪氨酸激酶B(TrKB)在大脑皮质及海马的表达特点。方法取出生2～5d豚鼠60只,随机分为3组,C组为对照组;T1组:腹腔注射晶体胆红素1mg·kg-1;T2组:腹腔注射晶体胆红素2mg·kg-1,分别在4h、8h处死。做脑组织切片,电镜、光镜观察其病理改变,并采用免疫组织化学、原位杂交和图像分析,观察不同时间点BDNFmRNA、TrKB在皮质及海马的表达变化。结果胆红素脑神经损伤模型成功建立。1.C组BDNFmRNA和TrKB在皮质及海马也有少量的表达;2.随时间延长和损伤加重,T1组和T2组皮质及海马的BDNFmRNA和TrKB表达明显上升,4h时T1组、T2组与C组比较,BDNFmRNA表达明显上升(P<0.05),T1组和T2组4h和8h比较,BDNFmRNA表达降低(P<0.05);3.TrKB在皮质和海马的表达也是随时间延长和损伤加重表达增加,4h、8h时T1组、T2组与C组比较,表达是增加的(P<0.05),T1组4h、8h与T2组8h比较,TrKB的表达是降低的(P<0.05)。结论胆红素脑神经损伤中,皮质和海马BDNFmRNA、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,有利于神经元修复和再生,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) mRNA and its receptor tyrosine kinase B (TrKB) in cerebral cortex and hippocampus of neonatal guinea pig with bilirubin-induced cranial nerve injury. Methods 60 guinea pigs from 2 to 5 days after birth were randomly divided into 3 groups: group C: control group; group T1: intraperitoneal injection of crystal bilirubin 1 mg · kg-1; group T2: intraperitoneal injection of crystal bilirubin 2 mg · kg- 1, were killed at 4h, 8h respectively. The pathological changes were observed by electron microscope and light microscope. Immunohistochemistry, in situ hybridization and image analysis were performed to observe the expression of BDNF mRNA and TrKB in cortex and hippocampus at different time points. Results The bilirubin brain injury model was successfully established. 1. The expression of BDNF mRNA and TrKB in cortex and hippocampus in group C were also decreased in a small amount; 2. The expression of BDNF mRNA and TrKB in cortex and hippocampus of group T1 and T2 were significantly increased with the prolongation of time and injury, The expression of BDNF mRNA in cortex and hippocampus was also increased (P <0.05). The expression of BDNF mRNA in cortex and hippocampus was also increased at 4h and 8h (P <0.05). Compared with T2 group, the expression of TrKB was decreased at 4h, 8h (P <0.05). Conclusions In bilirubin-induced craniocerebral injury, elevated cortical and hippocampal BDNF mRNA and TrKB may reduce neuronal damage and play an important role in inhibiting neuronal apoptosis and neuronal repair, which may be beneficial for neuronal repair and regeneration. One of the mechanisms of the body’s self-protection in the neuronal injury of the brain.