中文摘要：

目的 体外细胞水平研究人参皂苷Rg1在冈田酸（OkadaicAcid,OKA）诱导的阿尔兹海默病（Alzheimerdis-ease,AD）样神经毒性模型中的保护作用,并初步探索其作用机制。方法 选用PC12细胞模拟神经元,采用OKA造模的同时给予Rg1（1、5、10μmol·L-1-）,选用褪黑素（Melato-nin,Melat）10μmol·L-1-作为阳性对照。分别采用MTT、LDH法检测细胞存活率及死亡率,采用流式细胞术检测细胞凋亡情况,用DCFH-DA荧光探针法检测胞内ROS的堆积,并用试剂盒检测细胞内一系列抗氧化酶活性的变化。结果与对照组相比,OKA组细胞存活率明显降低、死亡率明显增加,细胞早期凋亡数量明显增多（P〈0.01）;氧化应激相关指标检测发现,OKA组胞内ROS堆积明显增多（P〈0.01）,总抗氧化能力（ABTS）JE明显降低（P〈0.01）,过氧化物酶（Catalase,CAT）（P〈0.01）,超氧化物歧化酶（Su-peroxide Dismutase,SOD）、谷胱甘肽过氧化物酶（Glutathione peroxidase,GSH-Px）活性都明显降低（P〈0.05）,GSSG/GSH比率明显升高（P〈0.01）。与模型组相比,Rg1不同剂量组均能显著提高OKA模型中PC12细胞的存活率,降低细胞死亡率,并抑制胞内ROS水平、提高抗氧化酶活力增强抗氧化能力。结论 人参皂苷Rg1在OKA诱导的AD样病理模型中可以通过抗氧化应激作用发挥抗细胞死亡、保护神经细胞的作用。

英文摘要：

Aim To the investigate the protective effect of ginsenoside Rg1 in Alzheimer＇s disease （ AD）-like neurotoxicity model induced by okadaic acid （ OKA） in the cellular level , and explore the mecha-nism preliminarily. Methods The PC12 cells model, simulate neurons, induced by OKA was given Rg1 （1, 5,10 μmol·L^-1）, and melatonin （Melat） 10 μmol·L^-1 was given as a positive control. MTT and LDH were carried out to assess the cell viability and mortality. To detect the accumulation of ROS, the DCFH-DA fluores-cent probe was conducted. And to assess the change of the activity of a variety of antioxidant enzymes, various kits were used, including ABTS、CAT、SOD、GSH-Px and GSSG/GSH. Results Compared with the control group, the survival rate of PC12 cell in OKA group re-duces significantly, the mortality rate was increased sig-nificantly , the number of early apoptotic cells was in-creased significantly （P〈0. 01）. Oxidative stress-relat-ed indicators show that ROS accumulation within the cells of OKA group increases significantly （ P〈0. 01 ） , and the total antioxidant capacity （ ABTS ） decreases significantly （ P 〈 0. 01 ） , the activity of peroxidase （Catalase, CAT） （P 〈0. 01）, glutathione peroxidase （glutathione peroxidase, GSH-Px） and superoxide dis-mutase （ superoxide dismutase, SOD） decreased signifi-cantly （ P 〈0. 05 ） , the rate of GSSG/GSH increased significantly （ P 〈0. 01 ） . Compared with the model group, the different doses of Rg1 could improve the sur-vival rate and decrease the mortality rate of PC12 cell significantly in the group of OKA, and could decrease the level of the accumulation of ROS, improve the activ-ity of antioxidant enzymes. Conclusion Ginsenoside Rg1 can decrease PC12 cell apoptosis by exerting an-tioxidant effects, and protect the nerve cells in AD-like pathology model induced by OKA.