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Effect of sinomenine on gene expression of the IL-1 beta-activated human synovial sarcoma.
Li, X J; Yue, Patrick Y K; Ha, W Y; Wong, Daisy Y L; Tin, Mandy M Y; Wang, P X; Wong, Ricky N S; Liu, L.
Afiliação
  • Li XJ; School of Chinese Medicine, Hong Kong Baptist University, Hong Kong.
Life Sci ; 79(7): 665-73, 2006 Jul 10.
Article em En | MEDLINE | ID: mdl-16566946
ABSTRACT
Sinomenine is an alkaloid with pharmacological effects of anti-inflammation, anti-angiogenesis, anti-arthritis and immunosuppression. This study aimed to investigate the effect of sinomenine on gene expression of human synovial sarcoma cells (Hs701.T) activated by IL-1 beta. The proliferative effect of sinomenine was examined in the presence or absence of IL-1 beta by the [3H]-thymidine incorporation and MTT assay, respectively. Using DNA microarray technology and RT-PCR, the activating action of IL-1 beta and modulatory effect of sinomenine on Hs701.T were simultaneously determined. Results showed that IL-1 beta could stimulate the proliferation and gene expression of Hs701.T cells. Sinomenine could significantly inhibit proliferation of IL-1 beta-activated Hs701.T cells and suppress expression of 17 genes including IL-6, PlGF, Daxx, and HSP27. These genes were found to be important in tumor progression through the mediation of inflammation, cell adhesion, proliferation, apoptosis and angiogenesis. In conclusion, our study provides supplementary information for the further studies on the pharmacological effects of sinomenine acting on synovial sarcoma.
Assuntos
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Bases de dados: MEDLINE Assunto principal: Sarcoma / Membrana Sinovial / Anti-Inflamatórios não Esteroides / Interleucina-1 / Morfinanos Limite: Humans Idioma: En Revista: Life Sci Ano de publicação: 2006 Tipo de documento: Article País de afiliação: Hong Kong
Buscar no Google
Bases de dados: MEDLINE Assunto principal: Sarcoma / Membrana Sinovial / Anti-Inflamatórios não Esteroides / Interleucina-1 / Morfinanos Limite: Humans Idioma: En Revista: Life Sci Ano de publicação: 2006 Tipo de documento: Article País de afiliação: Hong Kong