脑源性神经营养因子对缺氧缺血胚鼠脑细胞凋亡的作用

Effect of brain - derived neurotrophic factor on apoptosis of embryo brain suffered from intrauterine hypoxic - ischemic injury

目的探讨外源性脑源性神经营养因(BDNF)在宫内缺氧缺血环境下对胚鼠脑神经细胞凋亡的作用及其可能信号传导途径。方法 钳夹孕鼠子宫动脉30 min后,实验组经孕鼠尾静脉注射2 μg BDNF,对照组注入生理盐水、Tunel法测定各组脑组织神经细胞凋亡,免疫组织化学分析不同时间点胞外信号调节酶(ERK),c-Jun氨基末端激酶(JNK)表达情况。结果随缺血再灌注时间延长,胚脑凋亡细胞逐渐增多。实验组胚脑组织同时间点神经细胞凋亡数较对照组少,ERK表达较对照组增强,JNK表达成弱。结论BDNF在宫内缺氧缺血环境下有减少胚脑神经细胞凋亡作用,该作用可能与激活ERK信号途径有关。

Objective To investigate the effect and possible signal pathway of brain - derived neurotrophic factor (BDNF) on apoptosis of rat embryo brain cells suffering from intrauterine hypoxic - ischemic injury. Methods The uterine arteries of the pregnant rats were clamped for 30 minutes in both experimental group and control group. BDNF(2 μg) was injected into rats in experimental group while saline was injected into rats in control group through caudal veins. The samples were collected at 24, 48 and 72 hours re-spectively after artery clamping. Neuroapoptosis of different groups induced by ischemic damage was measured by TUNEL assay. The expression of extracellular signal - regulated kinase(ERK)and c - Jun - N - terminal kinase(JNK) were observed by immunohisloche-mistry.Results The number of apoptosis cells after hypoxic - ischemic injury increased progressively with time.The apoptosis cells number in experimental group were much lower in number than those of ischemic control group.The expression of ERK increased while the expression of JNK decreased in experimental group, comparing with that of the ischemic control group, with statistical signif-icance (P<0.05).Conclusions BDNF demonstrates neuroprotective effects on rat embryo brain cells suffering from intrauterine hy-poxic - ischemic injury; its mechanism may be associated with erecting antiapoptotic function on rat embryo brain cells through activat-ing the ERK signal pathway.