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Involvement of CDK4, pRB, and E2F1 in ginsenoside Rg1 protecting rat cortical neurons from beta-amyloid-induced
Xiao-Chun Chen1, Li-Min Chen, Yuan-Gui Zhu
1Fujian Institute of Geriatrics, Union Hospital, Fujian Medical University, Fuzhou 350001, China. xc-chen329@sohu.com
Aim:
To explore the possible mechanism of beta-amyloid (Abeta)-induced apoptosis in rat cortical neurons and the protective effect of ginsenoside Rg1.
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 E2F1 mRNA.
Results:
Treatment with Abeta1-40 at the concentration of 20, 40, 80 mg/L for 48 h induced rat cortical neuron apoptosis from 12.5 %+/-1.5 % (control) to 22.3 %+/-1.4 %, 38.8 %+/-1.3 %, 36.7 %+/-1.4 %, respectively. Pretreatment with Rg1 at the dose of 0.5, 1, 2, 4, 8, 16 micromol/L for 24 h, then treatment with Abeta1-40 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 Abeta1-40 40 mg/L for 24 h, there were transient increases in CDK4 and phosphorylated pRB protein level, as well as the expression of E2F1 mRNA. However, the above levels decreased markedly after pretreatment with Rg1 8 micromol/L for 24 h.
Conclusion:
Ginsenoside Rg1 attenuated Abeta1-40-induced apoptosis in rat cortical neurons via inhibiting the activity of CDK4, decreasing the phosphorylation of pRB and downregulating the expression of E2F1 mRNA.
Insights
Ginsenoside Rg1 protects rat cortical neurons from beta-amyloid-induced apoptosis by inhibiting CDK4 activity and downregulating E2F1 mRNA expression. This study reveals a novel mechanism for neuroprotection against Alzheimer's disease pathology.
Area of Science:
- Neuroscience
- Pharmacology
- Cell Biology
Background:
- Beta-amyloid (Abeta) is implicated in the pathogenesis of Alzheimer's disease.
- Abeta induces apoptosis in cortical neurons, contributing to neurodegeneration.
- Ginsenoside Rg1 is a traditional herbal medicine with potential neuroprotective properties.
Purpose of the Study:
- To investigate the mechanism of Abeta-induced apoptosis in rat cortical neurons.
- To evaluate the protective effect of ginsenoside Rg1 against Abeta-induced neuronal apoptosis.
Main Methods:
- Apoptosis was assessed using AO-EB staining and DNA fragmentation analysis.
- Cyclin-dependent kinases-4 (CDK4) and phosphorylated pRB levels were measured by Western blot.
- E2F1 mRNA expression was quantified using RT-PCR.
Main Results:
- Abeta1-40 significantly increased cortical neuron apoptosis.
- Ginsenoside Rg1 dose-dependently reduced Abeta1-40-induced apoptosis.
- Abeta1-40 transiently increased CDK4, phosphorylated pRB, and E2F1 mRNA, which were reversed by Rg1 pretreatment.
Conclusions:
- Ginsenoside Rg1 attenuates Abeta1-40-induced apoptosis in rat cortical neurons.
- The protective mechanism involves inhibiting CDK4 activity, decreasing pRB phosphorylation, and downregulating E2F1 mRNA expression.
