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

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. 6 h treatment of OGD most significantly decreased NSC viability, and 10-20 μM 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.