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• W3139014785 abstract "Abstract Bisphenol S (BPS) is associated with neurotoxicity, but its molecular mechanisms are unclear. Our aim was to investigate the role of the brain‐derived neurotrophic factor (BDNF)/tyrosine kinase B (TrkB)/cAMP‐response element‐binding protein (CREB) signaling pathway in BPS‐induced cytotoxicity in SK‐N‐SH cells. The cells were treated with various concentrations of BPS, and cell viability, apoptosis rate, mitochondrial membrane potential (MMP), and the BDNF, cleaved‐caspase‐3, B‐cell lymphoma 2 (Bcl‐2), Bcl‐2‐associated X protein (Bax), TrkB, CREB, and phospho‐CREB (p‐CREB) levels were determined. The effects of pretreatment with the TrkB activator 7,8‐dihydroxyflavone (7,8‐DHF) were also explored. BPS decreased SK‐N‐SH cell viability and altered their morphology. Their apoptosis rate was increased, as were the levels of the proapoptotic proteins Bax and cleaved‐caspase‐3, but MMP was decreased. Thus, BPS may induce mitochondria‐dependent apoptosis pathways. BPS also reduced the BDNF, TrkB, and p‐CREB levels, and pretreatment with 7,8‐DHF alleviated its cytotoxic effects. Thus, BPS‐induced cytotoxicity might be mediated by the BDNF/TrkB/CREB signaling pathway." @default.
• W3139014785 created "2021-03-29" @default.
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• W3139014785 date "2021-03-22" @default.
• W3139014785 modified "2023-09-27" @default.
• W3139014785 title "Role of the BDNF/TrkB/CREB signaling pathway in the cytotoxicity of bisphenol S in SK‐N‐SH cells" @default.
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• W3139014785 doi "https://doi.org/10.1002/jbt.22775" @default.
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