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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。结杲: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。
Objective: To observe the changes of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) in brain tissue of rats with acute global cerebral ischemia-reperfusion injury and the corresponding morphological changes of brain cells, and to explore the role of neurotrophic factor in global cerebral ischemia Reperfusion injury in the role. Methods: A rat model of acute global cerebral ischemia-reperfusion injury was established by Pulsinlli method. The content of NGF and BDNF in brain tissue was determined by enzyme linked immunosorbent assay (ELISA). The morphology of brain cells was observed under light microscope. Results: After reperfusion injury, the expression of BDNF and NGF in brain tissue were increased. The model group increased at 2 h after perfusion, peaked at 6 h, and then decreased at 24 h. Compared with the sham-operated group, there was a significant difference (P <0.01). Under light microscope, there were no abnormal nerve cells in sham-operation group. The abnormal nerve cells in each subgroup of model group increased significantly at 2 h after ischemia-reperfusion and the lightest at 6 h. The abnormal nerve receptors were prolonged with the reperfusion time Damage degree becomes heavier. CONCLUSION: Ischemia-reperfusion injury can induce the expression of BDNF and NGF, which is beneficial to the protection of neuronal injury after ischemia-reperfusion injury.