银杏叶提取物预处理对红藻氨酸致痫大鼠神经肽Y表达的影响

Influence of Ginkgo biloba extract pretreatment on neuropeptide Y expression of kainic acid induced epileptic rats

目的观察银杏叶提取物(GBE)预处理给药对癫痫大鼠的干预效应及其与神经肽Y(NPY)表达的关系,以探讨GBE的抗癫痫机制。方法雄性SD大鼠侧脑室注射红藻氨酸(KA)建立癫痫动物模型,将72只SD大鼠随机均分为假手术组(A组)、GBE对照组(B组)、癫痫模型组(C组)、GBE预处理组(D组),各组再分为造模成功后6、12、24 h处死这3个亚组,每个亚组6只大鼠。采用HE染色观察海马组织中神经元细胞形态变化,用免疫组织化学技术测定海马组织中NPY蛋白的表达。结果 D组大鼠癫痫发作级别及神经元损害较C组降低;C组3个亚组的大鼠海马组织中NPY蛋白表达较A组相对应的各亚组明显增多(P<0.05);D组中3个亚组大鼠海马组织中NPY蛋白的表达较C组相对应的各亚组明显增多(P<0.05);B组与C组相比相关指标均无统计学意义;同组内6、12、24 h 3个时间点NPY蛋白表达呈上升趋势。结论 GBE预处理给药有一定的抗癫痫作用,其抗癫痫的机制与减轻神经元的损害、减轻癫痫发作程度及NPY蛋白表达上调有关。

Objective To investigate the intervention effects of Ginkgo biloba extract （GBE） pretreatment on epi- leptic rats and its relationship with the expression of neuropeptide Y （ NPY）, and to probe the anti-epileptic mecha- nism of GBE. Methods An animal model of complex partial epilepsy was established in male SD rats by intracere- broventricular injection of kainic acid. 72 SD rats were randomly divided into sham operation group （ group A）, GBE control group （group B）, epilepsy model group （group C）, and GBE pretreatment group （group D）. Each group was further divided into three subgroups （6, 12 and 24 h after seisures）. Morphologic changes of the hipp- ocampal neurons were observed by HE staining, while the expressions of NPY in hippocampal tissue were measured by immunohistochemieal techniques. Results Seizure levels and neuronal damage of rats in group D were lower than those in group C. In hippocampal tisse, NPY expression of three subgroups in Group C increased significantly than those in group A （ P 〈 0. 05 ） ; NPY expressions of three subgroups of Group D increased significantly than those in group C （ P 〈 0. 05 ）. No statistically different NPY expression was found between group B and group C. Up-regulation of NPY expression was noted from 6 h to 24 h time point after seisures in the same group. Conclu- sion GBE pretreatment has some antiepileptic effects which are concerned with ameriolation of neuronic damage, the mitigation of seizure degree, and the up-regulation of NPY expression.