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TrkB基因在脑源性神经营养因子治疗宫内缺氧缺血性脑损伤中的表达变化
引用本文:李亚琴,韩树萍,王 玢,郭锡熔. TrkB基因在脑源性神经营养因子治疗宫内缺氧缺血性脑损伤中的表达变化[J]. 南京医科大学学报(自然科学版), 2008, 28(7): 841-844
作者姓名:李亚琴  韩树萍  王 玢  郭锡熔
作者单位:南京医科大学附属南京妇幼保健院儿科,江苏南京200004
基金项目:江苏省南京市医学科技发展基金
摘    要:目的:探讨酪氨酸激酶(TrkB)基因在尾静脉注射脑源性神经营养因子(BDNF)治疗官内缺血缺氧脑损伤中的表达变化.方法:钳夹孕鼠子宫动脉30 min后,尾静脉注射BDNF 1 μg或2 μg,持续5天,同时设立假手术组和生理盐水组为对照,RT-PCR和Western blot方法检测胎鼠TrkB mRNA和蛋白的表达变化.结果:孕鼠子宫动脉钳夹30 min后,可造成胎鼠TrkB的表达增高,并且进行尾静脉注射外源性BDNF可使TrkB表达增高更为明显.结论:通过尾静脉注射BDNF可明显上调胎鼠脑内TrkB的核酸和蛋白表达,加强BDNF对脑神经元的保护和修复作用.

关 键 词:脑源性神经营养因子  TrkB受体  缺血缺氧性脑损伤
收稿时间:2008-03-05

Effect of brain derived neurotrophic factor on TrkB mRNA and protein expression in embryonic rat brain suffered from intrauterine hypoxic-ischemic injury
LI Ya-qin,HAN Shu-ping,WANG Bin and GUO Xi-rong. Effect of brain derived neurotrophic factor on TrkB mRNA and protein expression in embryonic rat brain suffered from intrauterine hypoxic-ischemic injury[J]. Acta Universitatis Medicinalis Nanjing, 2008, 28(7): 841-844
Authors:LI Ya-qin  HAN Shu-ping  WANG Bin  GUO Xi-rong
Affiliation:Department of Pediatrics,Nanjing Maternity and Child Health Hospital Affiliated to NJMU,Nanjing 210004,China
Abstract:Objective:To investigate the effect of brain derived neurotrophic factor on TrkB mRNA and Protein expression in embryonic rat brain suffered from intrauterine hypoxic-ischemic injury.Methods:The uterine arteries of pregnant rats were clamped for 30 min,and saline or BDNF was injected to the rat through caudal veins for 5 days.Rats with sham surgery were used as controls.The expression of TrkB mRNA and protein was measured using RT-PCR and Western blotting.Results:TrkB mRNA and levels of protein expression were higher in embryonic rat brain after clamping the uterine arteries of pregnant rats for 30 min than those in control group.BDNF injection could up-regulate the TrkB expression significantly.Conclusion:BDNF injection through rat caudal veins could up-regulate the levels of the TrkB mRNA and protein expression in embryonic rat brain suffered from intrauterine hypoxic-ischemic injury and may enhance its neuroprotection effect on cortical neurons.
Keywords:brain derived neurotrophic factor  TrkB receptor  hypoxic ischemic brain damage
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