摘要
为了观察葛根素对血管性痴呆(VD)模型大鼠海马锥体细胞和BDNF表达的影响及其作用机制,本研究采用双侧颈总动脉缺血再灌注,同时腹腔注射硝普钠建立血管性痴呆大鼠模型,选出造模成功者随机分为模型组及葛根素干预组,各为24只,另以条件匹配的24只大鼠为假手术组。分别在造模术后15d,1、2和4个月等时间点,采用水迷宫检测大鼠学习记忆能力的变化,HE染色和免疫组化染色观察大鼠海马神经元的形态学改变及BDNF表达的变化。结果显示:(1)模型组大鼠的逃逸潜伏期(EL)均明显长于假手术组(P<0.01),葛根素干预组大鼠的EL较模型组明显缩短(P<0.05),但仍长于假手术组(P<0.05);(2)模型组大鼠海马CA1区锥体细胞数比假手术组明显减少(P<0.01),葛根素干预组2个月和4个月时点锥体细胞数较模型组明显增多(P<0.01),但仍少于假手术组(P<0.01);(3)模型组大鼠海马BDNF阳性细胞明显减少(P<0.01),除15d和1个月组DG区外,葛根素干预组大鼠海马BDNF阳性细胞数较模型组明显增多(P<0.05),但仍低于假手术组(P<0.05);(4)模型组大鼠海马BDNF阳性细胞平均吸光度值较假手术组明显降低(P<0.01),而葛根素干预组比模型组和假手术组均明显降低(P<0.05)。本研究结果提示,脑缺血再灌注后,海马BDNF阳性神经元和锥体细胞持续减少,在VD学习记忆障碍的发生和发展过程中起重要作用;葛根素对脑缺血再灌注损伤具有保护作用,其机制可能与葛根素上调BDNF的表达、减少锥体细胞的丢失有关。
To observe the effects of Puerarin （Pue） on hippocampal pyramidal cell and the expression of BDNF in vascular dementia rats and the relative mechanism, the vascular dementia （VD） rat models were established by repeatedly cerebral ischemia/reperfusion and were randomly divided into two groups： model group and Pue-treated group （ n =24 for each）, and another 24 condition-matched rats were selected as the sham-operated （SO） group. Morris water maze was used to detect the changes of learning and memory ability, and HE staining and immunohistechemical staining were used to observe the changes of neurons＇ morphology and BDNF expression in rat hippocampus. The results showed that： （ 1 ） The escape latency （EL） of model group was obviously longer than that of SO group at different point after VD modeling operation （P 〈0.01 ）, while the EL of Pue-treated group was significantly shorter than that of model group （ P 〈 0. 05 ）, but still longer than that of the SO group （ P 〈 0.01 ） ; （ 2 ） The numbers of pyramidal neurons in hippocampal CA1 area of model group were lower than that of SO group （ P 〈0.01 ）, while the numbers of pyramidal neurons in 2 and 4 month Pue-treated subgroups were more than that of model group （ P 〈 0.01 ）. But the numbers of Pue-treated were still lower than that of SO group （ P 〈 0.01 ） ; （ 3 ） Compared with the SO group, BDNF-pesitive neurons in the hippecampus of model group decreased significantly （P 〈 0.01 ）. The number of BDNF-pesitive neurons in hippocampus of Pue-treated group increased significantly than that of model groups（ P 〈0.05 ） except for the hipppcampal DG area at 15 days and 1 month groups, but still lower than that of SO group（ P 〈 0.05 ） ; （4） Compared with the SO group, the average absorbance （A） value of BDNF immunoreactive neurons in the model group was significantly lower （ P 〈 0.01 ）, and the average A value of Pue-treated group was significantly lower than that of model and SO groups （ P 〈0.05 ）. These results suggest that after cerebral ischemia/reperfusion, the continued decrease of the number of hippocampal pyramidal cells and BDNF-positive cells play an important role in the course of occurrence and development of VD rats; Pue has obvious role in brain protection of cerebral ischemia/reperfusion. The possible mechanism is that it can up-regulate the expression of BDNF and decrease the loss of pyramidal cell.
出处
《神经解剖学杂志》
CAS
CSCD
北大核心
2007年第6期615-620,共6页
Chinese Journal of Neuroanatomy
基金
山东省教育厅科研基金(NoJ01K09)资助项目
