ArticleNutrients2019
Equol Pretreatment Protection of SH-SY5Y Cells against Aβ (25-35)-Induced Cytotoxicity and Cell-Cycle Reentry via Sustaining Estrogen Receptor Alpha Expression.
Article in Nutrients, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Equol as a Multitarget Agent Against Neurodegeneration: Mechanistic Insights into Its Molecular Modulation.Neuromolecular medicine · 2025Review
- From the gut to the brain: the long journey of phenolic compounds with neurocognitive effects.Nutrition reviews · 2025Review
- Neuroprotective Potential of Indole-Based Compounds: A Biochemical Study on Antioxidant Properties and Amyloid Disaggregation in Neuroblastoma Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Alzheimer's Disease-Related Epigenetic Changes: Novel Therapeutic Targets.Molecular neurobiology · 2024Review
- Attenuation of estrogen and its receptors in the post-menopausal stage exacerbates dyslipidemia and leads to cognitive impairment.Molecular brain · 2023Article
- Deciphering the Mysterious Relationship between the Cross-Pathogenetic Mechanisms of Neurodegenerative and Oncological Diseases.International journal of molecular sciences · 2023Review
- Potential Protective Mechanisms of S-equol, a Metabolite of Soy Isoflavone by the Gut Microbiome, on Cognitive Decline and Dementia.International journal of molecular sciences · 2022Review
- Protective Effects of Flavonoids against Alzheimer's Disease: Pathological Hypothesis, Potential Targets, and Structure-Activity Relationship.International journal of molecular sciences · 2022Review
- Modifiable Innate Biology within the Gut-Brain Axis for Alzheimer's Disease.Biomedicines · 2022Review
- Review
- Recent Advances in Molecular Pathways and Therapeutic Implications Targeting Mitochondrial Dysfunction for Alzheimer's Disease.Molecular neurobiology · 2022Review
- Baicalin Attenuated ABioMed research international · 2022Article
- Autophagy and apoptosis cascade: which is more prominent in neuronal death?Cellular and molecular life sciences : CMLS · 2021Review
- Estrogenic hormones receptors in Alzheimer's disease.Molecular biology reports · 2021Review
- Down-regulation of cyclin D2 in amyloid β toxicity, inflammation, and Alzheimer's disease.PloS one · 2021Article
- Flavonoids as a Natural Enhancer of Neuroplasticity-An Overview of the Mechanism of Neurorestorative Action.Antioxidants (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
β-amyloid formation in the brain is one of the characteristics of Alzheimer's disease. Exposure to this peptide may result in reentry into the cell cycle leading to cell death. The phytoestrogen equol has similar biological effects as estrogen without the side effects. This study investigated the possible mechanism of the neuron cell-protecting effect of equol during treatment with Aβ. SH-SY5Y neuroblastoma cells were treated with either 1 μM S-equol or 10 nM 17β-estradiol for 24 h prior to 1 μM Aβ (25-35) exposure. After 24 h exposure to Aβ (25-35), a significant reduction in cell survival and a reentry into the cell cycle process accompanied by increased levels of cyclin D1 were observed. The expressions of estrogen receptor alpha (ERα) and its coactivator, steroid receptor coactivator-1 (SRC-1), were also significantly downregulated by Aβ (25-35) in parallel with activated extracellular signal-regulated kinase (ERK)1/2. However, pretreatment of cells with S-equol or 17β-estradiol reversed these effects. Treatment with the ER antagonist, ICI-182,780 (1 μM), completely blocked the effects of S-equol and 17β-estradiol on cell viability, ERα, and ERK1/2 after Aβ (25-35) exposure. These data suggest that S-equol possesses a neuroprotective potential as it effectively antagonizes Aβ (25-35)-induced cell cytotoxicity and prevents cell cycle reentry in SH-SY5Y cells. The mechanism underlying S-equol neuroprotection might involve ERα-mediated pathways.
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Registered trials
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.