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AIM: To explore the possible mechanism of β-amyloid (Aβ)-induced apoptosis in rat cortical neurons and the protective effect of ginsenoside Rg_1. METHODS: AO-EB staining was used to quantify the apoptotic cells. DNA fragmentation was observed by gel electrophoresis. The levels of cyclin-dependent kinases-4 (CDK4) and phosphorylated pRB were detected by Western blot. RT-PCR was used to examine the expression of E2FI mRNA. RESULTS: Treatment with Aβ_(1-40) at the concentration of 20, 40, 80 mg/L for 48 h induced rat cortical neuron poptosis from 12.5％±1.5％(control) to 22.3％±1.4％, 38.8％±1.3％, 36.7％±1.4％, respectively. Pretreatment with Rg_1 at the dose of 0.5, 1, 2, 4, 8, 16 μmol/L for 24 h, then treatment with Aβ_(1-40)40 mg/L for 24 h, the percentage of apoptotic neurons decreased from 38.8％±1.3％ to 14.5％±1.3％, 13.3％±1.0％, 11.6％±0.29％, 11.8％±1.0％, 6.2％±0.8％, 5.8％±0.8％, respectively. After treatment with Aβ_(1-40)40 mg/L for 24 h, there were transient increases in CD
AIM: To explore the possible mechanism of β-amyloid (Aβ) -induced apoptosis in rat cortical neurons and the protective effect of ginsenoside Rg_1. METHODS: AO-EB staining was used to quantify the apoptotic cells. DNA fragmentation was observed by gel electrophoresis . The levels of cyclin-dependent kinases-4 (CDK4) and phosphorylated pRB were detected by Western blot. RT-PCR was used to examine the expression of E2FI mRNA. RESULTS: Treatment with Aβ 1-40 at the concentration of 20 , 40, 80 mg / L for 48 h induced rat cortical neuron poptosis from 12.5% ± 1.5% (control) to 22.3% ± 1.4%, 38.8% ± 1.3%, 36.7% ± 1.4%, respectively. Pretreatment with Rg_1 at the dose of 0.5, 1, 2, 4, 8, 16 μmol / L for 24 h, then treatment with Aβ 1-40 40 mg / L for 24 h, the percentage of apoptotic neurons decreased from 38.8% ± 1.3% to 14.5% ± 1.3%, 13.3% ± 1.0%, 11.6% ± 0.29%, 11.8% ± 1.0%, 6.2% ± 0.8%, 5.8% ± 0.8% L for 24 h, there were transient increases in CD