人参皂苷Rd预处理对局灶性脑缺血再灌注大鼠NR2B受体和核酸内切酶G表达的影响  

Effect of Ginsenoside Rd Pretreatment on the Expressiom of NR2B Receptor and Endonuclease G After Focal Cerebral lschemia-Reperfusion in Rats

作　　者：杜旭辉[1] 杨金升[1] 石向群[1] 闫俊强[1] 

机构地区：[1]兰州军区兰州总医院神经内科,730050

出　　处：《国际脑血管病杂志》2008年第8期571-575,共5页International Journal of Cerebrovascular Diseases

摘　　要：目的：观察人参皂苷Rd预处理对局灶性脑缺血再灌注大鼠基底节区N-甲基-D-天冬氨酸（NMDA）受体亚单位NR2B蛋白和核酸内切酶G（EndoG）表达变化的影响，探讨人参皂苷Rd治疗缺血性卒中的可能机制。方法：栓线法建立大鼠大脑中动脉闭塞模型，免疫组织化学染色和图像分析法检测局灶性脑缺血1h再灌注1、6、24、72h后基底节区NR2B和FaxtoG表达，评价人参皂苷Rd对NR2B和EndoG表达和脑梗死体积的影响。结果：缺血再灌注组缺血侧基底节区NR2B阳性表达显著增加，EndoG在细胞核内表达显著；再灌注不同时间点人参皂苷Rd处理组NR2B和EndoG阳性表达均显著降低（P〈0．05或P〈0．01），脑梗死体积显著缩小（P〈0．01）。结论：脑缺血再灌注后NMDA受体亚单位NR2B和凋亡诱导因子EndoG表达显著增加；人参皂苷Rd预处理能显著降低NR2B和EndoG表达，通过抑制兴奋性神经毒性和阻断神经细胞凋亡，缩小脑梗死体积，从而起神经保护作用。Objective： To observe the effect of ginsenoside Rd pretreatment on the expressions of N-methyl-D-aspartate （NMDA） receptor subunit NR2B protein and endonuclease G （EndoG） in basal ganglia region after cerebral focal ischemia-reperfusion in rats and to investigate possible mechanism of ginsenoside Rd in the treatment of ischemic stroke. Methods： A rat model of middle cerebral artery occlusion （MCAO） was induced by intraluminal filament method. The expressions of NR2B and EndoG in basal ganglia region for focal cerebral ischemia 1 hour, and 1, 6, 24 and 72 hours reperfusion were detected by immunohistochemical staining and image analysis method. The effects of ginsenoside Rd on the expressions of EndoG and NR2B and the volurne of cerebral infarction were evaluated. Results： The positive expression of NR2B in basal ganglia region on the ischemic side in ischemia-reperfusion group was increased significantly. The expression of EndoG in the nucleus was notable; the positive expressions of NR2B and EndoG at different reperfusion time points in ginsenoside Rd pretreatment group were decreased significantly （P 〈 0. 05 or P 〈 0.01 ）, and the volurne of cerebral infarction was reduced significantly （P 〈 0.01 ）. Conclusions： The expressions of NMDA receptor subunit NR2B protein and apoptosis-inducing factor EndoG were increased significantly after cerebral focal ischemiareperfusion; ginsenoside Rd pretreatment may significantly reduce the expressions of NR2B and EndoG. It reduces the volume of cerebral infarction by inhibiting excitatory neurotoxicity and blocking neuronal apoptosis, and thus plays a role in neuroprotection.

关 键 词：人参皂苷RD 脑缺血 NR2B受体 核酸内切酶G 

分 类 号：R285.5[医药卫生—中药学]