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《Journal of Guangzhou University of Traditional Chinese Medicine》 2007-02
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In-Vitro Inhibitory Effect of Ginsenoside Rg1 on Aβ_(25-35)-Induced NG108-15 Apoptosis in alzheimer's Disease Cellular model

WU Lei1,CHEN Yunbo2,WANG Qi2,CHENG Shuyi2,LIANG Weixiong2,WEN Zehuai2(1.The Second Affiliated Hospital,Guangzhou University of TCM,Guangzhou 510405,China;2.DME Center,Institute of Clinical Pharmacology,Guangzhou University of TCM,Guangzhou 510405,China)  
【Objective】To observe the protective effect of ginsenoside Rg1 on neurons and to explore its mechanism in Alzheimer's disease(AD) cellular model.【Methods】With NG108-15 cell as the representative of neurons,AD cellular model was induced by β-amyloid protein 25-35(Aβ25-35).The optimal concentration and treating time of Aβ25-35 for the modeling as well as those of Rg1 for pretreatment were screened by monitoring the morphological changes of NG108-15 with invert microscope and the apoptotic rate with flow cytometer.Then the nuclear factor-kappaB (NFκB) activity marked by immunocytochemical method was detected with fluorescene microscope and DMR picture analysis,Bcl-2 expression assayed with SABC immunohistocheimal method,and caspase-3 activity assayed with microplate reader and caspase-3 colorimetric assay kit.【Results】Treated with 20μmol/L Aβ2535 for 24 hours,NG10-15 cell apoptosis can be induced successfully.NF-κB activity in 2?μmol/L Rg1 group was markedly increased and caspase-3 activity was obviously decreased(P0.01 as compared with the model group),and Bcl-2 expression was positive in Rg1 pretreatment group.【Conclusion】High-concentration aggregated Aβ25-35 can down-regulate NF-κB activity in neurons and induce cell apoptosis.The protective mechanism of Rg1 on neurons is associated with the up-regulation of Bcl2 and inhibition of caspase-3 by switching on the activation of NF-κB in neurons.
【Fund】: 广东省自然科学基金项目(编号:31479)
【CateGory Index】: R285.5
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