ArticleCurrent issues in molecular biology2024
Ginsenoside Re Regulates Oxidative Stress through the PI3K/Akt/Nrf2 Signaling Pathway in Mice with Scopolamine-Induced Memory Impairments.
Article in Current issues in molecular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Dapagliflozin ameliorates Alzheimer's disease in rats via stimulating the protective arm of renin angiotensin system and suppressing neuroinflammation.Inflammopharmacology · 2026Article
- Interactions Between Nutraceuticals and α-Synuclein Conformational States: Molecular Mechanisms and Neuroprotective Implications in Parkinson's Disease.International journal of molecular sciences · 2026Review
- Effects of a Natural Polyherbal Extract on Alleviating Scopolamine-Induced Memory Deficits in C57BL/6 Mice via Enhancing Cholinergic Function.Current issues in molecular biology · 2025Article
- Acceleration-Dependent Effects of Vibrotactile Gamma Stimulation on Cognitive Recovery and Cholinergic Function in a Scopolamine-Induced Neurotoxicity Mouse Model.Biomedicines · 2025Article
- Neuroprotective Potential of Phytocompounds in the Treatment of Dementia: The State of Knowledge from the Scopolamine-Induced Animal Model of Alzheimer's Disease.Current issues in molecular biology · 2025Review
- Ambroxol confers neuroprotection against scopolamine-induced Alzheimer's-like pathology by modulating oxidative stress, neuroinflammation, and cognitive deficits via Nrf-2/JNK/GSK-3β signaling pathways.Frontiers in aging neuroscience · 2025Article
- Neuroprotective effects of astaxanthin in a scopolamine-induced rat model of Alzheimer's disease through antioxidant/anti-inflammatory pathways and opioid/benzodiazepine receptors: attenuation of Nrf2, NF-κB, and interconnected pathways.Frontiers in pharmacology · 2025Article
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Authors and funding
4 authors.
Funding
Abstract
While Ginsenoside Re has been shown to protect the central nervous system, reports of its effects on memory in the model of scopolamine-induced memory impairment are rare. The aim of this study was to investigate the effects of Ginsenoside Re on scopolamine (SCOP)-induced memory damage and the mechanism of action. Male ICR mice were treated with SCOP (3 mg/kg) for 7 days and with or without Ginsenoside Re for 14 days. As evidenced by behavioral studies (escape latency and cross platform position), brain tissue morphology, and oxidative stress indicators after Ginsenoside Re treatment, the memory damage caused by SCOP was significantly ameliorated. Further mechanism research indicated that Ginsenoside Re inhibited cell apoptosis by regulating the PI3K/Akt/Nrf2 pathway, thereby exerting a cognitive impairment improvement effect. This research suggests that Ginsenoside Re could protect against SCOP-induced memory defects possibly through inhibiting oxidative stress and cell apoptosis.
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