黄芪甲苷对PC12细胞缺糖缺氧损伤的保护作用  

Protective Effect of Astragaloside Ⅳ on PC12 Cells Injured by Oxygen-Glucose Deprivation

作　　者：杨文亮[1] 宋玉[1] 赵灿灿[1] 谢欣梅[1] 庞晓斌[1] 杜冠华[2] 

机构地区：[1]河南大学药学院药物研究所 [2]中国医学科学院&北京协和医学院药物研究所国家药物筛选中心

出　　处：《神经药理学报》2015年第1期10-14,共5页Acta Neuropharmacologica

基　　金：国家自然科学基金项目(No.81273652)

摘　　要：目的:探究黄芪甲苷对PC12细胞缺糖缺氧损伤的保护作用并探讨其可能的作用机制。方法:体外培养PC12细胞,应用无糖Earle’s稀释Na2S2O4建立缺糖缺氧模型,尼莫地平做阳性对照,使用不同浓度的黄芪甲苷进行预保护。显微镜下观察细胞形态差异,以MTT法测定细胞活力,酶标法测定上清液中乳酸脱氢酶(lactate dehydrogenase,LDH)含量,Western Blot法测定B淋巴细胞瘤-2(B-cell lymphoma-2,Bcl-2)与Bcl-2相关X蛋白(Bcl-2 associated X protein,Bax)蛋白表达量。结果:黄芪甲苷能够提高PC12细胞在缺糖缺氧环境下的细胞存活率,降低LDH漏出量,能够增加Bcl-2蛋白的表达,降低Bax蛋白的表达,降低Bax/Bcl-2比值。结论:黄芪甲苷对PC12细胞的缺糖缺氧损伤具有一定的保护作用,其作用机制可能与其抑制细胞凋亡有关。Objective：To investigate the protective effect and mechanism of astragaloside Ⅳ on PC12 cells injured by oxygen-glucose deprivation. Methods：The oxygen-glucose deprivation model of PC12 cells was constructed with Na_2S_2O_4 diluted with glucose-free Earle＇s. PC12 cells were treated with different doses of astragaloside Ⅳ. Nimodipine was taken as a positive control. The cellular morphology difference was observed and the cell survival rate was detected with MTT method. The lactate dehydrogenase（LDH） concentration was determined with enzyme linked immunosorbent assay. The expression of Bcl-2 and Bax protein were detected by Western blot. Results：The oxygen glucose deprivation（OGD） model was successfully established. In contrast with the OGD group,astragaloside Ⅳ could increase the survival rate of PC12 cells and reduce LDH leakage. Astragaloside Ⅳ could also increase the expression of Bcl-2 protein and decrease the expression of Bax protein. Conclusion：Astragaloside Ⅳ could relieve the PC12 cell injury induced by OGD and the protective effect may be related to inhibiting cell apoptosis.

关 键 词：黄芪甲苷 PC12细胞 缺糖缺氧损伤 细胞凋亡 

分 类 号：R965[医药卫生—药理学]