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目的 探讨自发性高胆固醇血症小鼠 (NJS小鼠 )短暂性前脑缺血后脑组织中脑源性神经营养因子和促调之因子的表达与神经元凋亡和神经行为改变的相关性。方法 选择NJS小鼠 6 0只 ,分为对照组 15只 ,缺血再灌注 2 4h组 15只、72h组 15只、12 0h组 15只。分别测定神经行为学指标、脑组织中BDNF、BAX的表达和神经元凋亡数。结果 脑缺血再灌注后BDNF表达峰值出现较BAX早 ,但BAX表达较BDNF表达持续时间长。BDNF/BAX比值与神经元凋亡数呈负相关、与神经功能的恢复呈正相关。结论 短暂性前脑缺血后脑组织BDNF和BAX表达的比值与神经元的损伤相关 ,提示增加脑缺血后脑组织内BDNF的含量和延长其表达时间将有助于对抗BAX对神经元的损伤作用 ,从而减少神经元的凋亡和促进神经功能的康复。
Objective To investigate the correlation between the expression of brain-derived neurotrophic factor (BDNF) and pro-inflammatory cytokines in neurons and neurobehavioral changes in spontaneously hypercholesterolemic mice (NJS mice) after transient forebrain ischemia. Methods Sixty NJS mice were selected and divided into control group (n = 15), ischemia-reperfusion group (24 h), ischemia-reperfusion group (n = 15), 72h group (n = 15) and 12h group (n = 15). The neurobehavioral indexes, the expression of BDNF and BAX in brain tissue and the number of neuron apoptosis were determined respectively. Results The peak of BDNF expression appeared earlier than that of BAX after cerebral ischemia and reperfusion, but the expression of BAX was longer than that of BDNF. The ratio of BDNF / BAX was negatively correlated with the number of neuronal apoptosis and positively correlated with the recovery of neurological function. Conclusions The ratio of BDNF and BAX in brain tissue after transient forebrain ischemia is related to the damage of neurons. It suggests that increasing the content of BDNF and prolonging the expression of BDNF in brain tissue after cerebral ischemia will help to prevent the damage of BAX to neurons , Thereby reducing neuronal apoptosis and promoting neurological rehabilitation.