ArticleJournal of molecular neuroscience : MN2019
Ginsenoside Compound K Regulates Amyloid β via the Nrf2/Keap1 Signaling Pathway in Mice with Scopolamine Hydrobromide-Induced Memory Impairments.
Article in Journal of molecular neuroscience : MN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 64 citations in OpenAlex.
- Nrf2 as a therapeutic target of ginseng: A comprehensive review from preclinical evidence to clinical applications.Journal of ginseng research · 2026Review
- The Substrate-Engine Model of Ferroptosis: Stage-Specific Targeting of Acyl-CoA Synthetase Long-Chain Family Member 4 and 5‑Lipoxygenase in Alzheimer's Disease.ACS pharmacology & translational science · 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
- Regular Exercise with Panax Ginseng Supplementation Attenuates Arsenic-Induced Muscular Weakness and Neurobehavioral Changes in Mice.Neurotoxicity research · 2025Article
- Article
- Review
- The role of Panax ginseng in neurodegenerative disorders: mechanisms, benefits, and future directions.Metabolic brain disease · 2025Review
- Ginsenoside CK modulates glucose metabolism via PPARγ to ameliorate SCOP-induced cognitive dysfunction.Metabolic brain disease · 2025Article
- Pharmacological mechanisms and therapeutic prospects of plant metabolites from traditional Chinese medicine in regulating programmed cell death in Alzheimer's disease.Frontiers in pharmacology · 2025Review
- Ginsenoside Re Regulates Oxidative Stress through the PI3K/Akt/Nrf2 Signaling Pathway in Mice with Scopolamine-Induced Memory Impairments.Current issues in molecular biology · 2024Article
- Review
- Structural Characters and Pharmacological Activity of Protopanaxadiol-Type Saponins and Protopanaxatriol-Type Saponins from Ginseng.Advances in pharmacological and pharmaceutical sciences · 2024Review
- Active Compounds ofPharmaceuticals (Basel, Switzerland) · 2023Review
- Article
- Review
- Protective effects of ginseng and ginsenosides in the development of osteoarthritis (Review).Experimental and therapeutic medicine · 2023Review
- The Mitochondrial-Derived Peptide (MOTS-c) Interacted with Nrf2 to Defend the Antioxidant System to Protect Dopaminergic Neurons Against Rotenone Exposure.Molecular neurobiology · 2023Article
- American Ginseng for the Treatment of Alzheimer's Disease: A Review.Molecules (Basel, Switzerland) · 2023Review
- Therapeutic Candidates for Alzheimer's Disease: Saponins.International journal of molecular sciences · 2023Review
- Nrf2-mediated activation of HO-1 is required in the blocking effect of compound K, a ginseng saponin metabolite, against oxidative stress damage in ARPE-19 human retinal pigment epithelial cells.Journal of ginseng research · 2023Article
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Authors and funding
12 authors at 1 institution in 1 country.
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Abstract
The objective of this study was to investigate the neuroprotective and antioxidant effects of ginsenoside compound K (CK) in a model of scopolamine hydrobromide-induced, memory-impaired mice. The role of CK in the regulation of amyloid β (Aβ) and its capacity to activate the Nrf2/Keap1 signaling pathway were also studied due to their translational relevance to Alzheimer's disease. The Morris water maze was used to assess spatial memory functions. Levels of superoxide dismutase, glutathione peroxidase, and malondialdehyde in brain tissues were tested. Cell morphology was detected by hematoxylin and eosin staining and terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling assay. Immunohistochemistry and western blotting were used to determine expression levels of Nrf2/Keap1 signaling pathway-related factors and Aβ. Ginsenoside CK was found to enhance memory function, normalize neuronal morphology, decrease neuronal apoptosis, increase superoxide dismutase and glutathione peroxidase levels, reduce malondialdehyde levels, inhibit Aβ expression, and activate the Nrf2/Keap1 signaling pathway in scopolamine-exposed animals. Based on these results, we conclude that CK may improve memory function in scopolamine-injured mice by regulating Aβ aggregation and promoting the transduction of the Nrf2/Keap1 signaling pathway, thereby reducing oxidative damage to neurons and inhibiting neuronal apoptosis. This study suggests that CK may serve as a future preventative agent or treatment for Alzheimer's disease.
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Registered trials
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