大鼠急性脑缺血再灌注损伤中BDNF与NGF的变化

目的:观察急性全脑缺血再灌注损伤大鼠脑组织神经生长因子(NGF)、脑源性神经营养因子(BDNF)的变化及相应的脑组织细胞形态,探讨神经营养因子在全脑缺血再灌注损伤中的作用.方法:采用Pulsinlli法建立大鼠急性全脑缺血再灌注损伤模型,酶联免疫吸附试验(ELISA法)动态测定脑组织NGF、BDNF含量,石蜡切片行HE染色光镜下观察脑组织细胞形态.结果:再灌注损伤后,脑组织BDNF、NGF表达均增高.模型组于灌注2 h上升,6 h达高峰,24 h回落;与假手术组相比,有显著性差异(P＜0.01).光镜下观察,假手术组无异常神经细胞,模型组各亚组中异常神经细胞于缺血再灌注2 h时明显增加,6 h受损最轻,随缺血再灌注时间延长异常神经受损程度变重.结论:缺血再灌注损伤可诱导BDNF、NGF表达,有利于缺血再灌注损伤后神经元损伤的保护.

The expressions of BDNF and GNF in the rats after acute brain injury following complete cerebral Ischemia reperfusion

Objective: To observe the expressions of both BDNF and NGF in the brain tissues of rats after acute brain injury following complete cerebral ischemia reperfusion, in order to investigate the function of the neurotrophic factors against cerebral ischemia-reperfusion injury. Methods: The animal model of whole brain ischemia-reperfusion was performed by blocking four vessels of Pulsinelli- Brierley's. ELISA was used to detect the levels of BDNF and NGF in the brain tissues of the rats dynamically. The deformations of neurons were calculated and observed through optic microscope after HE staining. Result: The expressions of BDNF and NGF in the brain tissues of rats after cerebral ischemia reperfusion injury were re actively increased in model groups. They started to increase at the second hour and to the top at the 6th hour, reduce at the 24th. The number of abnormal neurons in group B increased significantly at all the above observed periods through the optic microscope, and the number of abnormal neurons increased slightly at the 6th hour. The number of abnormal neurons was gradually decreased with the time of reperfusion prolonged. However, there were not abnormal neurons in the group A. Conclusion:The expressions of BDNF and NGF are induced in the brain of rats after cerebral ischemia-reperfusion, and it is beneficial for the protection of brain neurons.