ArticleNeurochemical research2017
Oxabicycloheptene Sulfonate Protects Against β-Amyloid-induced Toxicity by Activation of PI3K/Akt and ERK Signaling Pathways Via GPER1 in C6 Cells.
Article in Neurochemical research, 2017. 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, 13 citations in OpenAlex.
- Beyond Estrogen: Unraveling the Complexities of Hormonal Signaling Pathways in Alzheimer's Disease and Their Implications for Precision Therapy.Molecular neurobiology · 2025Review
- Neuroprotection against beta-amyloid toxicity by the novel estrogen receptor modulator STX requires convergent signaling pathways.Frontiers in molecular neuroscience · 2025Article
- Protective Effects ofLife (Basel, Switzerland) · 2023Article
- Targeting the non-classical estrogen pathway in neurodegenerative diseases and brain injury disorders.Frontiers in endocrinology · 2022Review
- Estrogenic hormones receptors in Alzheimer's disease.Molecular biology reports · 2021Review
- Paeoniflorin ameliorates Aβ-stimulated neuroinflammation via regulation of NF-κB signaling pathway and Aβ degradation in C6 glial cells.Nutrition research and practice · 2020Article
- Selective Targeting of Non-nuclear Estrogen Receptors with PaPE-1 as a New Treatment Strategy for Alzheimer's Disease.Neurotoxicity research · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxabicycloheptene sulfonate (OBHS) is a novel bicyclic core selective estrogen receptor modulator (SERM) with estrogen receptor (ER) antagonistic-activity and anti-inflammatory activity. However, little is known about protective action of OBHS on neurodegenerative disorders. In the present study, OBHS demonstrated a remarkably protective effect against amyloid beta (Aβ) induced cytotoxicity via G-protein-coupled estrogen receptor 1 (GPER1) in rat astroglial cell line (C6). The C6 cell death induced by Aβ was decreased by OBHS (1 μM) treatment for 45 min. This rapid protective action was blocked by GPER1 specific antagonist or siRNA knockdown. Inhibitors of phosphatidylinositol 3-kinase (PI3k)/Akt and extracellular signal-regulated kinase (ERK) activation also exhibited similar effects as GPER1 antagonist in blocking the protective effects of OBHS. Moreover, the expression of anti-apoptotic protein Bcl-2 was also increased by OBHS as a consequence of the activation of GPER1-PI3K/Akt and ERK pathways. Additionally, the phenyl sulfonate moiety of OBHS played a vital role in producing GPER1's agonist property according to the molecular docking analysis. These findings suggest that OBHS provide protection directed at enhancing glial cell survival through the activation of GPER1, which, in turn, offers a novel insight into the molecular mechanisms behind the potential application of OBHS in treating Alzheimer's disease (AD).
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