The role of Toll-like receptor 4 on inflammation and Aβ formation in cortex astrocytes / 生理学报
Acta Physiologica Sinica
;
(6): 631-638, 2014.
Artigo
em Inglês
| WPRIM
| ID: wpr-255992
ABSTRACT
To investigate the role and possible molecular mechanism of astrocytes in inflammation and amyloid β-protein (Aβ) formation, in this research, by using LPS to stimulate cultured rat astrocytes in vitro with or without anti-Toll-like receptor 4 (TLR4) antibody pretreatment, we first detected the TLR4, TNF-α, IL-1β, β-amyloid precursor protein (β-APP) and β-site APP clearing enzyme 1 (BACE1) mRNA with real-time PCR, and TLR4, NF-κB/P65 protein in cultured astrocytes by Western blot, and then further probed the translocation of NF-κB/P65 using immunofluorescence and the contents of TNF-α, IL-1β and Aβ in culture supernatant through ELISA. We found that all of these indexes increased at different degrees after LPS-stimulation. However, if pretreatment with anti- TLR4 antibody, such stimulating effects of LPS on the nuclear translocation of NF-κB/P65 and TNF-α, IL-1β, Aβ contents in astrocytic culture supernatant were reduced significantly or disappeared in comparison with the group with only LPS-administration. Our results suggest that TLR4 in astrocytes might play an important role in the inflammation and Aβ formation through the TLR4/NF-κB signaling pathway, thus providing new knowledge and understanding of the inflammatory hypothesis of AD pathogenesis.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
RNA Mensageiro
/
Transdução de Sinais
/
Células Cultivadas
/
Córtex Cerebral
/
Astrócitos
/
Ácido Aspártico Endopeptidases
/
Fator de Necrose Tumoral alfa
/
Precursor de Proteína beta-Amiloide
/
Biologia Celular
/
Fator de Transcrição RelA
Limite:
Animais
Idioma:
Inglês
Revista:
Acta Physiologica Sinica
Ano de publicação:
2014
Tipo de documento:
Artigo
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