Effects of trichostatin A on the expressions of inflammatory cytokines and toll-like receptor 4 and the acetylation of nuclear factor-κB induced by lipopolysaccharide in macrophage / 生理学报
Acta Physiologica Sinica
;
(6): 651-656, 2012.
Artigo
em Chinês
| WPRIM
| ID: wpr-333158
ABSTRACT
The present study aims to explore the possible mechanisms that trichostatin A (TSA), a histone deacetylases inhibitor (HDACi), affects the inflammatory signaling pathways of lipopolysaccharide/toll-like receptor 4/nuclear factor-κB (LPS/TLR4/NF-κB). Murine macrophage cell line RAW264.7 cells were employed. MTT assay was used to assess cell viability. The contents of TNF-α, IL-1β and IL-6 in culture supernatant were assayed by enzyme-linked immunosorbent assay (ELISA). TLR4 expression and NF-κB/p65 (Lys310) acetylation were examined by Western blotting. DNA binding activity of NF-κB/p65 was detected by using TransAM(TM) NF-κB/p65 activity assay kit. The results showed that, compared with control group, which was treated by DMSO, the cells treated with TSA (20, 40, 80 ng/mL) showed decreased percentages of cell survival (P < 0.05). The contents of TNF-α, IL-1β and IL-6 in culture supernatant were all increased by LPS (100 ng/mL), whereas reduced by 40 ng/mL TSA pretreatment (P < 0.05). TSA pretreatment inhibited LPS-induced up-regulation of TLR4 protein expression. Acetylation of NF-κB/p65(Lys310), which was already increased by LPS, was further enhanced by TSA (P < 0.05). On the contrary, LPS-increased DNA binding activity of NF-κB/p65 was decreased by pretreatment with TSA (P < 0.05). The results suggest that TSA-induced anti-inflammation may be attributed to decreases in the expression of TLR4 and DNA binding activity of NF-κB/p65.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Farmacologia
/
Acetilação
/
Transdução de Sinais
/
Regulação para Cima
/
Linhagem Celular
/
Lipopolissacarídeos
/
Interleucina-6
/
Fator de Necrose Tumoral alfa
/
Fator de Transcrição RelA
/
Receptor 4 Toll-Like
Limite:
Animais
Idioma:
Chinês
Revista:
Acta Physiologica Sinica
Ano de publicação:
2012
Tipo de documento:
Artigo
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