脑源性神经营养因子及酪氨酸激酶BmRNA在胆红素神经损伤豚鼠皮质及海马表达变化的实验研究  

The expression of BDNF and TrkB mRNA in cerebral cotex and hippocampus in guinea pig kernicterus model

作　　者：何平[1] 朱萍[1] 祝大丽[1] 李水冰[2] 

机构地区：[1]昆明医学院第二附属医院儿科,云南昆明650101 [2]云南大学生命科学院,云南昆明650000

出　　处：《临床儿科杂志》2012年第1期75-79,共5页Journal of Clinical Pediatrics

基　　金：云南省教育厅重点基金资助项目(No.037Z520C)

摘　　要：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)及其受体酪氨酸激酶B的mRNA(TrkB mRNA)在大脑皮质及海马表达特点。方法取生后2～5 d的豚鼠60只,随机分为3组,每组各20只。T1组腹腔注射晶体胆红素100μg/g;T2组腹腔注射胆红素200μg/g;C组为对照组,腹腔注射生理盐水。分别在注射后4、8 h各处死10只。作脑组织切片,电镜、光镜观察病理改变;并采用免疫组化、原位杂交和图像分析,观察不同时间点BDNF、TrkB mRNA在皮质及海马表达变化。结果胆红素脑神经元损伤模型成功建立。在腹腔注射胆红素4 h时,皮质及海马的BDNF阳性细胞数降低,而TrkB mRNA阳性细胞数增加,与对照组比较差异均有统计学意义(P<0.05)。随时间延长至8 h时,皮质及海马的BDNF和TrkB mRNA阳性细胞数均较4 h时增加,差异有统计学意义(P均<0.05)。T2组与T1组比较,皮质和海马的BDNF和TrkB mRNA的阳性细胞数变化更明显。结论胆红素脑神经元损伤时,皮质和海马的BDNF、TrkB mRNA表达变化可能在抑制神经元凋亡和神经元修复中发挥重要作用,有利于减轻神经元损伤,以及神经元的修复和再生,这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 tyrosine kinase B mRNA （TrkB mRNA） in cerebral cortex and hippocampus in neonatal guinea pig kernicterus model. Methods Sixty guinea pig, 2 - 5 days old, were randomly divided into C group （control group）, T1 group （intraperitoneal injection of crystalline bilirubin 100 tzg/g）, T2 group （intraperitoneal injection of crystalline bilirubin 200 μg/ g）. The guinea pigs were slaughter at 4 and 8 hours after injection. The brain was taken out. The pathological changes were observed by electron microscopy and light microscopy. The expression of BDNF and TrkB mRNA in cerebral cortex and hippocampus at 4 h and 8 h were detected by immunohistochemistry, in situ hybridization histochemistry, and image analysis. Results The kemicterus model was successfully established. Four hours after injection, the BDNF positive cells decreased while the TrkB mRNA positive cells increased in cerebral cortex and hippocampus. Compared with C group, differences in both Tl and T2 group were significant. The BDNF positive ceils and the TrkB mRNA positive cells increased more 8 hours than 4 hours after injection. Meanwhile, the T2 group had a more obvious change than T, group. Conclusions In process of bilirubin neuronal damage, the expression of BDNF and TrkB mRNA in the cortex and hippocampus may play an important role in inhibition of the apoptosis of neuronal, and repair of the neuronal. It is beneficial in reducing neuronal damage, and repairing and regenerating of neuronal, which might be one of the self-protection mechanisms.

关 键 词：胆红素 脑源性神经营养因子 酪氨酸激酶B 豚鼠 

分 类 号：R363[医药卫生—病理学]