摘要
为证明大鼠肌源性神经营养因子对损伤神经的保护作用 ,本文观察了此因子对缺氧时体外培养的大鼠脊髓运动神经元Bcl-2表达的影响。本实验从成鼠和乳鼠骨骼肌中提取肌源性神经营养因子 ,取 10 0μl (0 .1μg/ml)加入培养的胚胎大鼠脊髓运动神经元的培养液中 ,对照组加入等量的 PBS。然后用液体石蜡封闭液面造成神经元缺氧损伤 ,3 d后行 Nissl染色和免疫组化反应 ,观察和计数大鼠脊髓运动神经元存活数以及 Bcl-2免疫反应阳性神经元数 ,并对 Bcl-2阳性神经元作平均光密度分析。结果发现 :经成鼠和乳鼠肌源性神经营养因子孵育的脊髓运动神经元缺氧后的神经元存活数、Bcl-2阳性神经元数以及平均光密度均明显高于对照组 ,但乳鼠肌源性神经营养因子的效果更好。提示 :大鼠肌源性神经营养因子能增强缺氧时脊髓运动神经元 Bcl-2的表达 ,抑制缺氧后运动神经元的死亡 。
The effects of muscle derived neurotrophic factor (MDNF) on Bcl 2 expression of rat spinal cord motoneurons after anoxia invitro were investigated. MDNF was respectively extracted from adult and neonatal rat, 100 μl MDNF(0.1 μg/ml) was added into culture medium for neurons from spinal cords of embryonic rats. The equal volume of PBS was added into the medium for control. Then liquid paraffin was added into the medium to create the anoxia injuried neurons. Three days later, spinal cord motoneurons were stained by Nissl method and immunohistochemical antiserum of Bcl 2 .The number of the living neurons and the mean optical densities of Bcl 2 immunoreactive (Bcl 2 IR) positive neurons were observed. It was found that the number and mean optical density of Bcl 2 IR motoneurons of spinal cord after anoxia were significantly increased in MDNF group, as compared with the control, the effects of MDNF from neonatal rat were better than the ones from adult rat. Our results showed that MDNF can increase Bcl 2 expression and decrease the death of cultured motoneurons after anoxia and MDNF from neonatal rat may protect motoneurons from the damage induced by anoxia in better degree than that from adult rat.
出处
《神经解剖学杂志》
CAS
CSCD
北大核心
2002年第1期47-50,W012,共5页
Chinese Journal of Neuroanatomy
