摘要
[目的]研究神经生长因子(NGF)对氧合血红蛋白(0xyHb)诱导的小鼠脑细胞Bcl-2和Bax表达的影响,进一步探讨OxyHb诱导细胞凋亡及NGF对神经元保护作用的可能机制。[方法]雄性健康ICR小鼠随机分为损伤组(24只)、损伤给药组(24只)及对照组(6只),脑皮层局部蛛网膜下腔注射OxyHb建立蛛网膜下腔出血的动物模型,尾静脉注射神经生长因子,使用免疫组织化学法检测Bcl-2、Bax表达的情况。[结果]注射OxyHb后,Bcl-2表达降低,Bax表达增加,在NGF给药组,Bcl-2表达增加,而Bax表达则明显降低。[结论]注射入小鼠局部脑组织蛛网膜下腔的OxyHb可引起小鼠神经细胞Bax表达增加,可能是诱导凋亡的一个主要原因,而静脉注射NGF可以抑制OxyHb诱导的Bax表达增加,其机制可能是通过与受体结合,从而增加Bcl- 2蛋白表达,降低Bax表达水平以实现其保护作用。
[Objective] To investigate the effect of nerve growth factor （NGF） on the expression of Bcl-2 and Bax induced by oxyhemoglobin and provide the theoretical foundation for understanding the mechanism underlying apoptosis and protective effect of NGF. [Methods] Oxyhemoglobin were injected into the local subarachnoid space of ICR mice to prepare the model of subarachnoid hemorrhge and NGF were given intravenously after injury in the NGF treated group. Im- munohistochemical staining was used to detect Bcl-2 and Bax. [Results] After OxyHb injection, the expression of Bcl-2 was decreased, while the expression of Bax increased and reached its summit in 6h . In NGF group, the expression of Bcl- 2 was significantly increased, while the expression of Bax positive cells were obviously decreased. [Conclusion] OxyHb in subarachnoid space can induce apoptosis in mouse neuronal cells in vivo. The increased expression of Bax after OxyHb injection into subarachnoid space may be one of the main reasons for apoptosis after subarachnoid hemorrhage. Administration of NGF might has a protective effect on neuronal apoptosis after subarachnoid hemorrhage via regulating the expression of Bcl-2 and Bax.
出处
《武警医学院学报》
CAS
2006年第6期568-570,573,F0002,共5页
Acta Academiae Medicinae CPAPF
