Lipopolysaccharide-enhanced early proliferation of insulin secreting NIT-1 cell is associated with nuclear factor-kappaB- mediated inhibition of caspase 3 cleavage / 中华医学杂志(英文版)
Chinese Medical Journal
;
(24): 3652-3656, 2011.
Artigo
em Inglês
| WPRIM
| ID: wpr-273997
ABSTRACT
<p><b>BACKGROUND</b>Increased levels of plasma lipopolysaccharide (LPS) have been found in obesity and diabetes patients. This study was to investigate the effect of LPS on pancreatic beta-cell viability and the involvement of caspase 3 in NIT-1 cell line.</p><p><b>METHODS</b>Mouse insulinoma NIT-1 cells were treated with LPS for the indicated time and dose. Cell viability was measured by cell counting kit-8 reagent. Toll-like receptor 4 (TLR4), caspase 3 and cleaved caspase 3 were detected by Western blotting. Insulin was determined by radioimmunoassay (RIA).</p><p><b>RESULTS</b>LPS promoted NIT-1 cell proliferation at 1 µg/ml, peaked at 72 hours of incubation. A reduction in cleavage of caspase 3 was observed upon LPS treatment. Bay11-7082, a specific inhibitor of nuclear factor (NF)-κB, blunted LPS-induced inhibition of caspase 3 cleavage. Reduction in chronic insulin secretion was observed after treatment with LPS at 1 µg/ml for 48 and 72 hours, not for 24 hours. TLR4 protein was upregulated when NIT-1 cells were treated with LPS at 1 µg/ml for 24 hours.</p><p><b>CONCLUSIONS</b>LPS promotes early NIT-1 cell proliferation in association with NF-κB-mediated inhibition of caspase 3 cleavage. LPS exerts a time-dependent inhibitory effect on chronic insulin secretion from NIT-1 cells.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Farmacologia
/
Lipopolissacarídeos
/
NF-kappa B
/
Secreções Corporais
/
Linhagem Celular Tumoral
/
Proliferação de Células
/
Receptor 4 Toll-Like
/
Caspase 3
/
Insulina
/
Insulinoma
Limite:
Animais
Idioma:
Inglês
Revista:
Chinese Medical Journal
Ano de publicação:
2011
Tipo de documento:
Artigo
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