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ORIGINAL ARTICLE
Year : 2020  |  Volume : 16  |  Issue : 71  |  Page : 630-636

Effect and mechanism of ginsenoside Rg1 on synaptic plasticity of oxygen-glucose deprivation/reoxygenation-induced neuronal injury


1 Department of Pharmacology And Toxicology, Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine; Department of Traditional Chinese Medicine, Tianjin Vocational College of Bioengineering, Tianjin, China
2 Department of Acupuncture, Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China
3 Department of Pharmacology And Toxicology, Tianjin State Key Laboratory of Modern Chinese Medicine; Department of Clinical Research Evaluation, Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China
4 Department of Traditional Chinese Medicine, School of Chinese Materia Medica, Tianjin University of Traditional Chinese Medicine, Tianjin, China

Correspondence Address:
Xiang Fan
#10 Boyanghu Road, Jinghai District, Tianjin 301617
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/pm.pm_541_19

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Background: Ginsenoside Rg1 is the primary bioactive component of ginseng, which is a famous traditional Chinese medicine used to treat ischemic cardiovascular and cerebrovascular diseases. It has demonstrated considerable protective effects in neurons injured by ischemia/reperfusion both in in vitro and in vivoconditions. However, the effect and mechanism of action of ginsenoside Rg1 on the neural synaptic plasticity injured by ischemia/reperfusion have not yet been clarified. 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.


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