ArticleMolecules (Basel, Switzerland)2019
Ginsenoside Re Inhibits ROS/ASK-1 Dependent Mitochondrial Apoptosis Pathway and Activation of Nrf2-Antioxidant Response in Beta-Amyloid-Challenged SH-SY5Y Cells.
Article in Molecules (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 87 citations in OpenAlex.
- Traditional Chinese medicine ginseng regulates neurotrophic factors to improve neurodegenerative diseases: A potential strategy for Alzheimer's disease treatment.Journal of ginseng research · 2026Review
- Nrf2 as a therapeutic target of ginseng: A comprehensive review from preclinical evidence to clinical applications.Journal of ginseng research · 2026Review
- Ginsenoside Re Attenuates D-Galactose-Induced Aging-like Oxidative Stress in Cultured Bovine Oocytes via Activation of the SIRT1/Nrf2 Signaling Pathway.International journal of molecular sciences · 2026Article
- Ginsenoside Re mitigates AβJournal of ginseng research · 2026Article
- Roles of 670 nm Photobiomodulation on Rat Anterior Ischemic Optic Neuropathy: Enhancing RGC Survival, Mitochondrial Function, and Anti-Inflammatory Response.Antioxidants (Basel, Switzerland) · 2025Article
- Alzheimer's Disease Pathogenic Mechanisms: Linking Redox Homeostasis and Mitochondria-Associated Metabolic Pathways Through Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2).Antioxidants (Basel, Switzerland) · 2025Review
- The biological functions of ginsenoside and its applications in animal husbandry.Frontiers in veterinary science · 2025Review
- Pedunculoside alleviates cognitive deficits and neuronal cell apoptosis by activating the AMPK signaling cascade.Chinese medicine · 2024Article
- 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
- Korean red ginseng suppresses mitochondrial apoptotic pathway in denervation-induced skeletal muscle atrophy.Journal of ginseng research · 2024Article
- Active Compounds ofPharmaceuticals (Basel, Switzerland) · 2023Review
- A Qualitative Analysis of Cultured Adventitious Ginseng Root's Chemical Composition and Immunomodulatory Effects.Molecules (Basel, Switzerland) · 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
- Neural regeneration research model to be explored: SH-SY5Y human neuroblastoma cells.Neural regeneration research · 2023Article
- The Role of Fucoxanthin as a Potent Nrf2 Activator via Akt/GSK-3β/Fyn Axis against Amyloid-β Peptide-Induced Oxidative Damage.Antioxidants (Basel, Switzerland) · 2023Article
- Natural Products as Modulators of Nrf2 Signaling Pathway in Neuroprotection.International journal of molecular sciences · 2023Review
- Natural antioxidants that act against Alzheimer's disease through modulation of the NRF2 pathway: a focus on their molecular mechanisms of action.Frontiers in endocrinology · 2023Review
- Vitamin B3 Provides Neuroprotection via Antioxidative Stress in a Rat Model of Anterior Ischemic Optic Neuropathy.Antioxidants (Basel, Switzerland) · 2022Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Accumulation of amyloid-β (Aβ), which results in the formation of senile plaques that cause oxidative damage and neuronal cell death, has been accepted as the major pathological mechanism of Alzheimer's disease (AD). Hence, inhibition of Aβ-induced oxidative damage and neuronal cell apoptosis represents the effective strategies in combating AD. Ginsenoside Re (Re) has pharmacological effects against Aβ-induced neurotoxicity. However, its molecular mechanism remains elusive. The present study evaluated the effect of Re against Aβ-induced cytotoxicity and apoptosis in SH-SY5Y cells, and investigated the underlying mechanism. We demonstrate that Re inhibits the Aβ-triggered mitochondrial apoptotic pathway, as indicated by maintenance of mitochondrial functional, elevated Bcl-2/Bax ratio, reduced cytochrome c release, and inactivation of caspase-3/9. Re attenuated Aβ-evoked reactive oxygen species (ROS) production, apoptosis signal-regulating kinase 1 (ASK1) phosphorylation, and JNK activation. ROS-scavenging abrogated the ability of Re to alter ASK-1 activation. Simultaneously, inhibition of JNK abolished Re-induced Bax downregulation in Aβ-challenged SH-SY5Y cells. In addition, Re enhanced activation of the nuclear factor-E2-related factor 2 (Nrf2) in Aβ-induced SH-SY5Y cells. Knockdown of Nrf2 by small interfering RNA targeting Nrf2 abolished the protective effect of Re. Our findings indicate that Re could be a potential therapeutic approach for the treatment of AD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.