The protective effects of Ginsenosides Rg1 in AD-like pathological model induced by okadaic acid / 中国药理学通报

ABSTRACT

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.