Protective effects of ginsenoside Rg1 against oxygen-glucose-deprivation-induced apoptosis in neural stem cells

Jan 30, 2017Journal of the neurological sciences

Ginsenoside Rg1 may protect neural stem cells from damage caused by lack of oxygen and glucose

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Abstract

10-20μM ginsenoside Rg1 efficiently protected neural stem cells (NSCs) against oxygen-glucose deprivation (OGD) insult.

Oxygen-glucose deprivation significantly decreased NSC viability after 6 hours of exposure.
Ginsenoside Rg1 treatment reduced OGD-induced apoptosis in NSCs, as confirmed by staining techniques.
The expression of pro-apoptotic proteins cleaved Caspase3 and Bax was decreased with ginsenoside Rg1 treatment.
An increase in the anti-apoptotic protein Bcl-2 was observed in NSCs treated with ginsenoside Rg1 compared to those subjected to OGD.
Ginsenoside Rg1 also reduced oxidative stress and inhibited the phosphorylation of specific signaling proteins associated with stress responses.

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Oxygen-glucose deprivation (OGD) causes neural damages through stroke-induced ischemia. Neural stem cells (NSCs) have been shown to alleviate ischemia-induced neural damages. However, ischemia reduces NSC survival. Ginsenoside Rg1 exerts anti-inflammatory and anti-oxidative effects, and repairs brain injury-related neural damages. We aimed to investigate whether ginsenoside Rg1 could prevent NSCs from OGD insult. Using multiple techniques, we explored neuroprotective effects of ginsenoside Rg1 on OGD-insulted NSCs. 6h treatment of OGD most significantly decreased NSC viability, and 10-20μM ginsenoside Rg1 efficiently protected NSCs against OGD insult. Annexin V-FITC/propidium iodide (PI) double staining results confirmed that ginsenoside Rg1 significantly reduced the OGD-induced apoptosis in NSCs. OGD-insulted NSCs with ginsenoside Rg1 treatment displayed reduced expressions of pro-apoptotic proteins cleaved Caspase3 and Bax, and elevated expression of anti-apoptotic protein Bcl-2 than the NSCs with OGD insult. Moreover, ginsenoside Rg1 reduced OGD-induced oxidative stress, and inhibited the expression of p-p38 and p-JNK2. Ginsenoside Rg1 protects NSCs against OGD-induced cell apoptosis through regulating the expression of apoptotic signal proteins. In addition, ginsenoside Rg1 attenuates OGD-induced oxidative stress and inhibits p38/JNK2 phosphorylation in NSCs. Our study provides solid evidence for neuroprotective effects of ginsenoside Rg1 and reveals the underlying mechanisms.

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Protective effects of ginsenoside Rg1 against oxygen-glucose-deprivation-induced apoptosis in neural stem cells

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