脑源性神经营养因子对谷氨酸损伤神经元保护作用的研究  

Study on the protective effects of brain-derived neurotrophic factor on glutamate-injured neurons

作　　者：王虔[1] 程焱[1] 吴伟[1] 梁浩[1] 张瑞珠[1] 

机构地区：[1]天津医科大学总医院神经病学研究所,天津300052

出　　处：《中华老年心脑血管病杂志》2006年第1期57-60,共4页Chinese Journal of Geriatric Heart,Brain and Vessel Diseases

摘　　要：目的观察低剂量、短时程谷氨酸损伤的致凋亡作用及脑源性神经营养因子(brain derived neurotrophic factor,BDNF)对此损伤的反应及保护作用。方法体外培养大鼠皮质神经元并建立低剂量短时程谷氨酸损伤模型;以重组腺病毒分别于损伤前、后转导外源性BDNF;用Western blot检测BDNF和Bcl-2的表达情况;用原位末端标记法(TUNEL)检测神经元凋亡的情况。结果损伤后神经元凋亡率由对照组的17.8%上升至59.6%;重组腺病毒于损伤前、后转导BDNF可分别使BDNF的表达量上升至对照组的2.29倍和1.54倍,Bcl-2的表达量上升至对照组的1.72倍和1.32倍,细胞凋亡率降至30.8%和43%。结论腺病毒转导的外源性BDNF可保护谷氨酸损伤神经元免于凋亡;内、外源性BDNF均可诱导Bcl-2表达增高,腺病毒转导的外源性BDNF可保护谷氨酸损伤神经元免于凋亡;内、外源性BDNF均可诱导Bcl-2表达增高。Objectives To observe the apoptogenic effect of low-dosage and short-course glutamate injury and the response and protective effect of brain-derived nettrotrophic factor （BDNF） against the injury.Methods The model of injury was established with in vitro cultured conical neurons of neonatal rats. Heterogeneous BDNF was transducted into the neurons by adenovirus vector either before or after the injury. The expression levels of beth homo- and heterogeneous BDNF as well as Bcl-2 were examined by Western Blotting, and the apoptotic level by TUNEL. Results After glutamate injury, the apoptotic rate increased from the control level of 17.8% to 59.6%. After adenovirus transduction before and after the injury, the expression levels of BDNF increased to 2.29 and 1.54 folds of the control level respectively and Bcl-2 to 1.72 and 1.32 folds respectively, while the apoptotic rate dropped to 30.8% and 43% .Conclusions Glutamate injury really induces neuronal apoptosis and promotes the expression of homogeneous BDNF. Heterogeneous BDNF transducted by adenovirus vectors can be expressed properly not only before but also after the injury. Both homo- and heterogeneous BDNF induce the expression of Bcl-2. Heterogeneous BDNF can protect neurons against apoptosis.

关 键 词：脑源性神经营养因子 谷氨酸 神经元 细胞凋亡 

分 类 号：R741[医药卫生—神经病学与精神病学]