Effect and Mechanism of Ginsenoside Rg1 on Synaptic Plasticity of Oxygen‑Glucose Deprivation/Reoxygenation‑Induced Neuronal Injury

Objective: In this study, we aim to establish the model of oxygen–glucose deprivation/reoxygenation (OGD/ R)‑injured primary cortical neurons to mimic ischemia/reperfusion injury and investigate the mechanisms of action of ginsenoside Rg1 on the neural synaptic plasticity. Materials and Methods: Protective effects of ginsenoside Rg1 on neurons after OGD/R injury were measured by cell counting kit‑8, lactate dehydrogenase, and apoptosis assay. The mRNA expression and activity of growth associated protein (GAP)‑43, microtubule‑associated protein (MAP)‑2, Tau, insulin like growth factors (IGF)‑1, brain derived neurotrophic factor (BDNF), and vascular endothelial growth facto r (VEGF) in neurons after OGD/R injury were measured by real‑time polymerase chain reaction (RT‑PCR) or enzyme‑linked immunosorbent assay. The expression of apoptosis‑related genes and cytosolic Ca2+ levels in neurons were determined via RT‑PCR or Rhod‑2 fluorescence staining. Results: According to our results, ginsenoside Rg1 protected the neurons and promoted axonal regeneration and neuronal remodeling after OGD/R injury; increased the expression of GAP‑43, MAP‑2, Tau, IGF‑1, BDNF, VEGF, and Bcl‑2 and inhibited the expression of Bax; and decreased the intracellular Ca2+ overload in OGD/R‑injured neurons. Conclusion: Ginsenoside Rg1 can promote axonal regeneration and neuronal remodeling after OGD/R injury by upregulating the expression of synaptic remodeling proteins and endogenous neurotrophic factors, inhibiting intracellular Ca2+ overload and regulating the expression of apoptotic genes.