BACKGROUND:Modern pharmacological studies have shown that Ginsenoside Rg1 is one of the active components of ginseng that promote intelligence in the nervous system.Ginsenoside Rg1 can improve memory and learning in mouse models ofβ-amyloid protein(Aβ)-induced dementia. OBJECTIVE:To investigate whether effects of Ginsenoside Rg1 against Aβare associated with activity of nuclear factor-kappa B(NF-κB). DESIGN,TIME AND SETTING:The randomized,controlled,cell biological experiment was performed at the DME Center,Institute of Clinical Pharmacology,Guangzhou University of Chinese Medicine,China from July 2005 to May 2006. MATERIALS:Beta-amyloid fragment 25-35(Aβ_(25-35)) was supplied by the Neural Biochemical Laboratory,Xuanwu Hospital,Capital Medical University,China.Ginsenoside Rg1 was obtained from National Institute for the Control of Pharmaceutical and Biological Products,China.Rabbit anti-rat NF-κB p65 antibody was purchased from Santa Cruz Biotechnology,USA. METHODS:Hippocampal neurons and cortical astrocytes of neonatal Sprague Dawley rats were harvested and treated with various concentrations(0,5,10,20,and 40μmol/L) of Aβfor 6,12,and 24 hours to establish cellular models of Alzheimer’s disease.Cellular models were pretreated with various concentrations of Ginsenoside Rg1(1,2,4,8,and 16μmol/L).According to cell morphology and activity,the following conditions were selected:40μmol/L Aβfor 24 hours,as well as 2,4,and 8μmol/L Ginsenoside Rg1.NF-κB activity was observed using immunofluorescence and cytochemical staining. MAIN OUTCOME MEASURES:Morphology and viability of hippocampal neurons and cortical astrocytes,and activities of NF-κB were measured. RESULTS:Hippocampal neuron activity was significantly greater in the normal and 2 and 4μmol/L Ginsenoside Rg1 groups compared with the model group(P<0.05).Astrocyte activity was significantly greater in the normal,1,2,4,8,and 16μmol/L Ginsenoside Rg1 groups compared with the model group(P<0.05).NF-κB activity of hippocampal neurons was significantly greater in the normal,2,4,and 8μmol/L Ginsenoside Rg1 groups compared with the model group(P<0.01). NF-κB activity of astrocytes was significantly less in the normal,2,4,and 8μmol/L Ginsenoside Rg1 groups compared with the model group(P<0.01 or P<0.05).No significant difference in NF-κB activity was determined between the 2μmol/L Ginsenoside Rg1 and normal groups(P>0.05). CONCLUSION:Ginsenoside Rg1 protected neural cells by upregulating NF-κB activity in neurons and downregulating NF-κB activity in astrocytes.Ginsenoside Rg1(2μmol/L) maintained cell activity and NF-κB activity at normal levels. BACKGROUND: Modern pharmacological studies have shown that Ginsenoside Rg1 is one of the active components of ginseng that promote intelligence in the nervous system.Ginsenoside Rg1 can improve memory and learning in mouse models ofβ-amyloid protein(Aβ)-induced dementia. OBJECTIVE:To Discussion whether effects of Ginsenoside Rg1 against Aβare associated with activity of nuclear factor-kappa B(NF-κB). DESIGN,TIME AND SETTING:The randomized,controlled,cell biological experiment was performed at the DME Center,Institute of Clinical Pharmacology,Guangzhou University of Chinese Medicine, China from July 2005 to May 2006. MATERIALS: Beta-amyloid fragment 25-35 (Aβ_(25-35)) was supplied by the Neural Biochemical Laboratory, Xuanwu Hospital, Capital Medical University, China.Ginsenoside Rg1 was Obtained from National Institute for the Control of Pharmaceutical and Biological Products, China. Rabbit anti-rat NF-κB p65 antibody was purchased from Santa Cruz Biotechnology, USA. METHODS: Hippocampal n Eurons and cortical astrocytes of neonatal Sprague Dawley rats were harvested and treated with various concentrations(0,5,10,20,and 40μmol/L) of Aβfor 6,12, and 24 hours to establish cellular models of Alzheimer’s disease.Cellular models were Pretreated with various concentrations of Ginsenoside Rg1(1,2,4,8,and 16μmol/L).According to cell morphology and activity,the following conditions were selected:40μmol/L Aβ for 24 hours,as well as 2,4,and 8μmol/L Ginsenoside Rg1.NF-κB activity was observed using immunofluorescence and cytochemical staining. MAIN OUTCOME MEASURES: Morphology and viability of hippocampal neurons and cortical astrocytes, and activities of NF-κB were measured. RESULTS: Hippocampal neuron activity was significantly greater in The normal and 2 and 4μmol/L Ginsenoside Rg1 groups compared with the model group (P<0.05). Astrocyte activity was significantly greater in the normal, 1,2,4,8, and 16μmol/L Ginsenoside Rg1 groups compared with the model Group(P<0.05).NF-κB acti Vity of hippocampThe neurons were significantly greater in the normal, 2,4,and 8μmol/L Ginsenoside Rg1 groups compared with the model group (P<0.01). NF-κB activity of astrocytes was significantly less in the normal,2,4,and 8μmol /L Ginsenoside Rg1 groups compared with the model group (P<0.01 or P<0.05). No significant difference in NF-κB activity was determined between the 2μmol/L Ginsenoside Rg1 and normal groups (P>0.05). CONCLUSION: Ginsenoside Rg1 Protective neural cells by upregulating NF-κB activity in neurons and downregulating NF-κB activity in astrocytes. Ginsenoside Rg1 (2 μmol/L) maintained cell activity and NF-κB activity at normal levels.