Role of the BDNF/TrkB/CREB signaling pathway in the cytotoxicity of bisphenol S in SK-N-SH cells.
J Biochem Mol Toxicol
; 35(6): 1-11, 2021 Jun.
Article
em En
| MEDLINE
| ID: mdl-33749030
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.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Fenóis
/
Sulfonas
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Glicoproteínas de Membrana
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Transdução de Sinais
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Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico
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Fator Neurotrófico Derivado do Encéfalo
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Receptor trkB
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Citotoxinas
Limite:
Humans
Idioma:
En
Ano de publicação:
2021
Tipo de documento:
Article