慢性脑灌注不足老龄大鼠脑内BDNF的表达

Expression of brain-derived neurotrophic factor in the brain of old rats after chronic cerebral perfusion deficiency

目的 探讨老龄大鼠慢性灌注不足后脑内脑源性神经营养因子 (brain derivedneurotrophic ,BDNF)的表达在血管性痴呆形成中的作用。方法 采用Pulsinelli四血管阻断 ( 4 vesselocclusion ,4VO)改良法建立血管性痴呆大鼠模型 ,穿梭箱系统检测大鼠的学习记忆能力。应用免疫组化ABC法检测海马各区及额、颞叶皮层BDNF的表达。结果 4VO 1周组海马CA1区BDNF阳性细胞数与对照组比较显著减少 (P <0 .0 1) ,2周组、4周组仍进行性下降 (P <0 .0 1) ,2月组与 4周组无显著差异 (P >0 .0 5 )。CA1区BDNF的表达与大鼠AAR成绩变化规律基本一致。 3d组额、颞叶皮层BDNF表达显著增加 ,1周组CA3、齿状回及颞叶皮层BDNF显著减少 (P <0 .0 1) ,而后BDNF的表达无明显变化。

Objective To explore the roles of expression of brain derived neurotrophic factor (BDNF) in the brain of old rats after chronic cerebral perfusion deficiency in the pathogenesis of vascular dementia. Methods Rat model of vascular dementia was established by modified Pulsinelli 4 vessel occlusion (4VO) and divided into 3d (3 d), 1 week (1 w), 2 weeks (2 w), 4 weeks (4 w) and 2 months (2 m) groups. Computer controlled initiative avoidance response shuttle box system was used to test the learning and memory capacity of rats. Immunohistochemical method was used to examine the expression of BDNF in CA1 region of the hippocampus and cortex of temporal and frontal lobe. Results Compared with those in control group, BDNF positive cells in CA1 region were decreased significantly in 4VO 1 w group ( P <0 01), and then decreased gradually in 4VO 2 w and 4VO 4 w groups ( P <0 01). There was no significant difference in 4VO 2 m and 4VO 4 w groups ( P >0 05). Compared with those in the control group, BDNF positive cells in the cortex of temporal and frontal lobe were increased significantly in 4VO 3 d group ( P <0.01). BDNF positive cells in hippocampus CA3 region and dentate gyrus and the cortex of temporal lobe were decreased significantly in 4VO 1 w group ( P <0.01), and then came to a stable state. Conclusion The decreased expression of BDNF in brain regions correlated with the cognitive functions of old rats after chronic cerebral perfusion deficiency may be an important pathological mechanism in the formation of vascular dementia, especially in the hippocampus CA1 region.