Objective It is to investigate the effect and mechanism of tetrahydroxy stilbeneglucoside (TSG),Tenuigenin (TEN) and their combination to anti-PC12 cells damaged by Aβ25-35.Methods PC12 cell induced by Aβ25-35 was established Alzheimer's disease damage models,and these PC12 cells were randomly divided into normal group,model group(20 μ mol/L Aβ25-35),TSG group(100 μmol/L TSG),TEN group(50 μmol/L TEN),TSG + TEN group(100 μ mol/L TSG + 50 μmol/L TEN) by factorial design.Each group had 6 complex holes.The cells survival rate,Acetylcholine-sterase (AchE) activity,Superoxide dismutase (SOD) activity,Malei-c Dial-dehyde (MDA) content,and cell differentiation rate of each group were detected or counted.Results Compared with the model group,the cells survival rate,SOD activity and cell differentiation rate were higher while the AchE activity and MDA content were lower in TSG group,TEN group and TSG + TEN group (P ＜ 0.05).Moreover,from high to low in the order about the cells survival rate and cell differentiation rate were:TSG + TEN group,TSG group and TEN group(P ＜0.05).From high to low in the order about the AchE activity was:TSG + TEN group,TSG group and TEN group(P ＜ 0.05).The SOD activity of TSG group was higher than the TEN group(P ＜ 0.01),and the AchE activity and MDA content of TSG + TEN group and TSG group were lower while SOD activity was higher than that of TEN group (P ＜ 0.05),no significant difference in SOD activity and MDA content was found between TSG + TEN group and TSG group.Conclusion The combination of TSG and TEN had an obvious synergy to anti-PC12 cells damaged by synergy Aβ25-35,and the protection for PC12 cells of TSG was more obvious than TEN.The synergy mechanism of TSG uniting TEN may be related to improving the nervous cholinergic system function and protecting the nerve cells in the synaptic plasticity,but had nothing to do with the effect of oxidative stress system.The protection of TSG for PC12 cells was more obvious than TEN,the mechanism may be related to the more obvious improvement of TSG in the nervous cholinergic system function,nerve antioxidant stress function and he nerve cells in the synaptic plasticity.%目的 探讨二苯乙烯苷(TSG)、远志皂苷元(TEN)及二者合用对Aββ25-35损伤PC12细胞的保护作用及相关机制.方法 PC12细胞采用Aβ325-35诱导建立阿尔茨海默病的损伤模型.用析因设计,设立正常组、模型组(20 μmol/L Aββ25-35)、TSG组(100 μmol/L TSG)、TEN组(50 μmol/L TEN)、TSG+ TEN组(100 μmol/L TSG+ 50 μmol/L TEN),每组分设6个复孔.检测各组细胞存活率、乙酰胆碱酯酶(AchE)活力、超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量,统计各组细胞分化率.结果 TSG组、TEN组及TSG+ TEN组细胞存活率、SOD活力及细胞分化率均明显高于模型组(P均＜0.05),AchE活力、MDA含量均明显低于模型组(P均＜0.05).且细胞存活率、细胞分化率从高到低依次为TSG+ TEN组、TSG组、TEN组(P均＜0.05),AchE活力从低到高依次为TSG+ TEN组、TSG组、TEN组(P均＜0.05).TSG组和TSG+ TEN组AchE活力和MDA含量均明显低于TEN组(P均＜0.05),SOD活力均明显高于TEN组(P均＜0.05),TSG+ TEN组SOD活力和MDA含量与TSG组比较差异均无统计学意义(P均＞0.05).结论 TSG与TEN合用抗Aβ25-35损伤PC12细胞具有明显协同作用,机制可能与明显改善神经胆碱能系统功能、保护神经细胞突触可塑性有关,而与对氧化应激系统的影响关系不显著;TSG对PC12细胞的保护作用优于TEN,机制可能与TSG改善神经胆碱能系统功能、神经细胞抗氧化应激功能及保护神经细胞突触可塑性的作用较TEN显著有关.
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