ISGF3, a critical factor of the IFN-alpha pathway in the antiviral action of HBV / 中华实验和临床病毒学杂志
Chinese Journal of Experimental and Clinical Virology
;
(6): 110-113, 2005.
Artículo
en Chino
| WPRIM
| ID: wpr-333088
ABSTRACT
<p><b>OBJECTIVE</b>To study the mechanism of signal transduction in anti-HBV action of IFN-alpha.</p><p><b>METHODS</b>The HBV DNA in HepG 2.2.15 cell line supernatant with/without IFNalpha-2b were monitored by fluorescence real-time quantitive PCR. STAT1, STAT2, ISGF3-gamma, PKR, 2'5'-OAS mRNA levels from HepG 2 and HepG 2.2.15 cell lines that were treated with/without IFNalpha-2b at different times were detected by semi-quantitive RT-PCR. And the ISGF3-gamma protein was detected by Western blot. Then, these items were detected again after inhibiting the JAK-STAT pathway with genistein.</p><p><b>RESULTS</b>The HBV DNA in 2215 supernatant that were treated with IFNalpha-2b for 8 hours decreased 0.72 log 10 copies/ml. But the basal levels of DNA in cells pretreated with genistein? followed by IFNalpha-2b did not decrease. The STAT1, STAT2, ISGF3-gamma, 2'5'-OAS, PKR mRNA levels were upregulated by IFNalpha-2b. The same phenomena were observed with STAT1, STAT2, ISGF3-gamma mRNA when pretreated with genistein then treated with IFNalpha-2b, but the levels of 2'5'-OAS, PKR mRNA were decreased in this situation. The expression of the protein of ISGF3-gamma was also augmented by IFNalpha-2b, and was blocked by genistein.</p><p><b>CONCLUSION</b>The JAK-STAT pathway seems to be a critical pathway in IFNalpha-2b action against HBV? and ISGF3 is most probably a key factor of the route.</p>
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Antivirales
/
Farmacología
/
ADN Viral
/
ARN Mensajero
/
Transducción de Señal
/
Regulación Neoplásica de la Expresión Génica
/
Virus de la Hepatitis B
/
Western Blotting
/
Reacción en Cadena de la Polimerasa
/
Interferón-alfa
Tipo de estudio:
Guía de Práctica Clínica
Límite:
Humanos
Idioma:
Chino
Revista:
Chinese Journal of Experimental and Clinical Virology
Año:
2005
Tipo del documento:
Artículo
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