牛蒡子苷元对阿尔茨海默病体外模型细胞凋亡和氧化损伤的影响

Arctigenin Inhibits Cell Apoptosis and Oxidative Damage in an in Vitro Model of Alzheimer′s Disease

目的:探讨牛蒡子苷元对阿尔茨海默病体外模型β淀粉样肽25-35(Aβ_(25-35))诱导PC12细胞凋亡和氧化损伤的影响及机制。方法:将PC12细胞分成对照组、模型组(Aβ_(25-35)处理)、ATG-L组(2μmol/L牛蒡子苷元和Aβ_(25-35)处理)、ATG-M组(4μmol/L牛蒡子苷元和Aβ_(25-35)处理)、ATG-H组(8μmol/L牛蒡子苷元和Aβ_(25-35)处理)、ATG-H+LY29400组(AKT信号抑制剂LY29400、8μmol/L牛蒡子苷元和Aβ_(25-35)处理)。以流式细胞术检测细胞凋亡变化,黄嘌呤氧化法检测超氧化物歧化酶(SOD)含量,Western Blotting法检测磷酸化的蛋白激酶B(p-AKT)蛋白表达。结果:ATG-L组、ATG-M组、ATG-H组p-AKT/AKT表达量以及SOD含量高于模型组,差异均有统计学意义(均P<0.05);ATG-L组、ATG-M组、ATG-H组细胞凋亡率低于模型组,差异均有统计学意义(均P<0.05);ATG-H+LY29400组p-AKT/AKT表达量以及SOD含量低于ATG-H组,差异均有统计学意义(均P<0.05);ATG-H+LY29400组细胞凋亡率高于ATG-H组,差异均有统计学意义(均P<0.05)。结论:牛蒡子苷元通过激活AKT信号通路抑制阿尔茨海默病体外模型Aβ_(25-35)诱导PC12细胞凋亡和氧化损伤。

Objective:To investigate the effect and its mechanis of arctigenin on the apoptosis and oxidative damage of PC12 cells induced by amyloid beta 25-35(Aβ25-35)in an in vitro model of Alzheimer′s disease.Methods:PC12 cells were divided into a control group,a model group(Aβ25-35 treatment),a ATG-L group(2μmol/L arctigenin and Aβ25-35 treatment),a ATG-M group(4μmol/L arctigenin and Aβ25-35 treatment),a ATG-H group(8μmol/L arctigenin and Aβ25-35 treatment),and a ATG-H+LY29400 group(AKT signal inhibitor LY29400,8μmol/L arctigenin and Aβ25-35 treatment).Flow cytometry was used to detect cell apoptosis changes.Xanthine oxidation method was used to detect superoxide dismutase(SOD)content.The expression of Phosphorylated protein kinase B(p-AKT)protein in cells was detected with Western Blotting method.Results:P-AKT/AKT expression and SOD content in the ATG-L,ATG-M,ATG-H group were higher than those in the Model group,and the differences were statistically significant(P s<0.05);The apoptosis rate of the ATG-L,ATG-M,ATG-H group were lower than those of the Model group,and the difference was statistically significant(P s<0.05);The p-AKT/AKT,SOD levels in the ATG-H+LY29400 group were lower than those in the ATG-L,ATG-M and ATG-H group,and the differences were statistically significant(P s<0.05);The apoptosis rate in the ATG-H+LY29400 group were higher than those in the ATG-H group,and the differences were statistically significant(P s<0.05).Conclusion:Arctigenin can inhibit the apoptosis and oxidative damage of PC12 cells induced by Aβ25-35 in an in vitro model of Alzheimer′s disease by activating the AKT signaling pathway.