Effects of nuclear factor-kappa B p65 ASODN on transforming growth beta-1 and intercellular adhesion molecule-1 of rat hepatic stellate cells / 中华肝脏病杂志
Chinese Journal of Hepatology
;
(12): 762-766, 2008.
Artigo
em Chinês
| WPRIM
| ID: wpr-279682
ABSTRACT
<p><b>OBJECTIVE</b>To study the effects of nuclear factor (NF)-kappa B p65 ASODN on transforming growth factor beta-1 (TGF beta 1) and intercellular adhesion molecule-1 (ICAM-1) of rat hepatic stellate cells (HSC) and the mechanisms of NF-kappa B p65 ASODN in treating liver fibrosis.</p><p><b>METHODS</b>Type IV collagen enzyme digestion and density centrifugation methods were used to separate rat hepatic stellate cells. NF-kappa B p65 ASODN was manually synthesized and completely phosphorothioate-modified. The changes of TGF beta 1 and ICAM-1 mRNA were detected by RT-PCR and albumen of TGF beta 1 and ICAM-1 were detected by ELISA. The changes of NF-kappa B activity were determined by ELISA.</p><p><b>RESULTS</b>NF-kappa B activity and the expressions of ICAM-1 and TGF beta 1 increased after the HSC were treated by TNF alpha. NF-kappa B activity weakened after being treated with NF-kappa B p65 ASODN (0.001-1.000 micromol/L), P less than 0.05 in a dose dependent manner. Transferring NF-kappa B p65 ASODN (0.001-1.000 micromol/L) also weakened the expression of ICAM-1 and TGF beta 1 mRNA and the protein induced by TNF alpha in HSC. It was also in a dose dependent manner, P less than 0.05.</p><p><b>CONCLUSIONS</b>After transferring NF-kappa B p65 ASODN into HSC, their NF-kappa B activity decreased, and their mRNA and protein expressions of ICAM-1 and TGF beta 1 also decreased. This may serve as a new way in treating hepatic fibrosis.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Farmacologia
/
Linhagem Celular
/
Oligonucleotídeos Antissenso
/
Fator de Necrose Tumoral alfa
/
Ratos Sprague-Dawley
/
Molécula 1 de Adesão Intercelular
/
Fator de Transcrição RelA
/
Fator de Crescimento Transformador beta1
/
Células Estreladas do Fígado
/
Genética
Limite:
Animais
Idioma:
Chinês
Revista:
Chinese Journal of Hepatology
Ano de publicação:
2008
Tipo de documento:
Artigo
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