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

Chen Yan; Yan Ma; Lin Li; Meng Zhang; Junhua Zhan; Xiang Fan

Articles

Abstract

Pharmacognosy Magazine,2020,16,71,630-636.

DOI:10.4103/pm.pm_541_19

Published:October 2020

Type:Original Article

Authors:

Author(s) affiliations:

Chen Yan¹, Yan Ma², Lin Li³, Meng Zhang⁴, Junhua Zhan³, Xiang Fan³
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

Abstract:

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.