Ginsenoside Rd Protects Neurons Against Glutamate-Induced Excitotoxicity by Inhibiting Ca2+ Influx

@article{Zhang2011GinsenosideRP,
  title={Ginsenoside Rd Protects Neurons Against Glutamate-Induced Excitotoxicity by Inhibiting Ca2+ Influx},
  author={Chen Zhang and Fang Du and Ming Shi and Ruidong Ye and Haoran Cheng and Junliang Han and Lei Ma and Rong Cao and Zhi-ren Rao and Gang Zhao},
  journal={Cellular and Molecular Neurobiology},
  year={2011},
  volume={32},
  pages={121-128}
}
Our previous studies have demonstrated that ginsenoside Rd (GSRd), one of the principal ingredients of Pana notoginseng, has neuroprotective effects against ischemic stroke. However, the possible mechanism(s) underlying the neuroprotection of GSRd is/are still largely unknown. In this study, we treated glutamate-injured cultured rat hippocampal neurons with different concentrations of GSRd, and then examined the changes in neuronal apoptosis and intracellular free Ca2+ concentration. Our MTT… Expand
Gastrodin Inhibits Glutamate-Induced Apoptosis of PC12 Cells via Inhibition of CaMKII/ASK-1/p38 MAPK/p53 Signaling Cascade
TLDR
Findings indicate that gastrodin protects PC12 cells from the apoptosis induced by glutamate through a new mechanism of the CaMKII/ASK-1/p38 MAPK/p53-signaling pathway. Expand
Protopanaxadiol ginsenoside Rd protects against NMDA receptor-mediated excitotoxicity by attenuating calcineurin-regulated DAPK1 activity
TLDR
The present study provided the first evidence that Rd could exert an inhibitive effect on NMDAR-triggered currents and sequential excitotoxicity through mitigation of DAPK1-mediated NR2b phosphorylation by attenuating calcineurin activity. Expand
Ginsenoside-Rd attenuates TRPM7 and ASIC1a but promotes ASIC2a expression in rats after focal cerebral ischemia
TLDR
The results suggest that ginsenoside (GS)-Rd neuroprotection following cerebral ischemia may be at least due to its effects on the expression of TRPM7, ASIC1a and ASIC2a. Expand
Paeoniflorin Attenuates Cerebral Ischemia-Induced Injury by Regulating Ca2+/CaMKII/CREB Signaling Pathway
TLDR
PF not only significantly decreased neurological deficit scores and infarct volume in vivo, but also improved neurons' cell viability, and inhibited neurons’ apoptosis and intracellular Ca2+ concentration in vitro. Expand
Ginsenoside Rd Protects Against Cerebral Ischemia–Reperfusion Injury Via Decreasing the Expression of the NMDA Receptor 2B Subunit and its Phosphorylated Product
TLDR
GSRd significantly improved the behavior score, infarct volume, and viability of the cultured neurons after ischemia, and inhibited the hyperphosphorylation of NR2B subunit and decreased the expression levels in cell membrane but did not change their levels in the total proteins after IRI. Expand
Ginsenoside Rd as a potential neuroprotective agent prevents trimethyltin injury.
TLDR
Ginsenoside Rd attenuated the tremor seizures and cognitive decline in behavioral tests and prevented TMT-induced cell apoptosis via regulation of B-cell lymphoma 2 (Bcl-2), bcl- 2-like protein 4 and caspase-3. Expand
Pseudoginsenoside-F11 Protects against Transient Cerebral Ischemia Injury in Rats Involving Repressing Calcium Overload
TLDR
This study indicates that PF11 produced neuroprotection and improved long-term outcomes while repressing calcium overload in model of transient focal ischemia, suggesting thatPF11 might be a considerable candidate for stroke treatment. Expand
Ginsenoside Rd Attenuates Mitochondrial Permeability Transition and Cytochrome c Release in Isolated Spinal Cord Mitochondria: Involvement of Kinase-Mediated Pathways
TLDR
It is concluded that Rd regulate mitochondrial permeability transition pore formation and cytochrome c release through protein kinases dependent mechanism involving activation of intramitochondrial Akt and ERK pathways. Expand
Cytoprotective effects of ginsenoside Rd on apoptosis-associated cell death in the isolated human pancreatic islets
TLDR
GS-Rd inhibited the progress of death of cultured human pancreatic islets by diminishing the apoptosis of the islet cells. Expand
Gastrodin protects against glutamate-induced ferroptosis in HT-22 cells through Nrf2/HO-1 signaling pathway.
  • Ting Jiang, Hui Cheng, +4 authors Qinglin Li
  • Medicine, Chemistry
  • Toxicology in vitro : an international journal published in association with BIBRA
  • 2019
TLDR
Results show that GAS protects HT-22 cells from the ferroptosis induced by glutamate through a new mechanism of Nrf2/HO-1 signaling pathway. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 42 REFERENCES
Neuroprotective effects of ginsenoside Rd against oxygen-glucose deprivation in cultured hippocampal neurons
TLDR
GSRd exhibited remarkable neuroprotection when presented during OGD and reoxygenation, which may be ascribed to its antioxidative properties by reducing the intracellular reactive oxygen species and malondialdehyde production; increasing glutathione content; and enhancing the antioxidant enzymatic activities of catalase, superoxide dismutase and glutATHione peroxidase. Expand
Chitooligosaccharides protect cultured hippocampal neurons against glutamate-induced neurotoxicity
TLDR
It is suggested that COSs prevent cultured hippocampal neurons from glutamate-induced cell damage by interfering with an increase in [Ca(2+)](c) and inhibiting caspase-3 activity. Expand
Ginsenosides Rb1and Rg3protect cultured rat cortical cells from glutamate‐induced neurodegeneration
TLDR
Results show that ginsenosides Rb1 and Rg3 exerted significant neuroprotective effects on cultured cortical cells, suggesting that these compounds may be efficacious in protecting neurons from oxidative damage that is produced by exposure to excess glutamate. Expand
Protective effects of ginsenoside Rg2 against glutamate-induced neurotoxicity in PC12 cells.
TLDR
The study suggests that ginsenoside Rg2 has a neuroprotective effect against glutamate-induced neurotoxicity through mechanisms related to anti-oxidation and anti-apoptosis and the inhibitory effect of ginseno-Rg2 against the formation of Abeta1-40 suggests that the drug may also represent a potential treatment strategy for Alzheimer's disease. Expand
Ginsenoside Rd attenuates mitochondrial dysfunction and sequential apoptosis after transient focal ischemia
TLDR
It is demonstrated that ginsenoside Rd exerts neuroprotective effects in transient focal ischemia, which may involve an integrated process of the mitochondrial protection, energy restoration and inhibition of apoptosis. Expand
Neuroprotective effect of individual ginsenosides on astrocytes primary culture.
TLDR
Ginsenosides from P. ginseng induce neuroprotection mainly through activation of antioxidant enzymes to reduce astrocytic death and increase ROS formation, ginsenoside Re being the most active. Expand
Inhibitory effect of ginsenosides on NMDA receptor-mediated signals in rat hippocampal neurons.
TLDR
Examination of the direct modulation of ginseng on the activation of glutamate, especially NMDA, receptors in cultured hippocampal neurons suggests that the inhibition of NMDA receptors by gINSeng, in particular by ginsenoside Rg3, could be one of the mechanisms for ginsENG-mediated neuroprotective actions. Expand
Protective effects of ginsenoside Rd on PC12 cells against hydrogen peroxide.
TLDR
It is suggested that ginsenoside Rd may be considered a potential antioxidant agent and should encourage further research in neurodegenerative diseases to explore the potential neuroprotective effects of ginsene Rd. Expand
Ginsenoside Rd attenuates early oxidative damage and sequential inflammatory response after transient focal ischemia in rats
TLDR
It is demonstrated that ginsenoside Rd exerts neuroprotection in transient focal ischemia, which may involve early free radicals scavenging pathway and a late anti-inflammatory effect. Expand
Calcium, ischemia and excitotoxicity.
TLDR
It is suggested that blocking certain receptors and ion channels is unlikely to be a useful therapeutic strategy due to potential deleterious side effects, however, identifying those that are most responsible for cell death and their downstream signalling pathways may lead to improved strategies for treating ischemic and excitotoxic disorders. Expand
...
1
2
3
4
5
...