作者: Jeffrey A. Moshier , Milton G. Mutchnick , Julie Dosescu , Todd K. Holtz , Sami Akkary
DOI: 10.1016/S0168-8278(96)80283-2
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摘要: Abstract Background: Thymosin-α 1 is a biological response modifier that has been used clinically, alone and in combination with interferon-α for the treatment of chronic hepatitis B viral infection. Both immunomodulatory immediate intracelluilar mechanisms have postulated to explain effect these two agents on HBV-infected hepatocytes. Methods: In this study, transfected HepG2 hepatoblastoma cells (HepG2-Nu2), derived from 2.2.15 cells, were as an vitro model determine efficacy thymosin-α interferon-α, individually combined, proliferation inhibitors cells. For comparison, parental SV40-transfected cell line (HepG2P9T2) also evaluated. Results: clonogenic soft agar assay, inhibited anchorage-independent growth HepG2-Nu2 by 40% compared untreated controls, but did not inhibit or HepG2P9T2 clonal growth. The was dose dependent over concentrations spanning three log units. 10 000 units/ml HepG2, HepG2-N4Z 33%, 41% 87%, respectively. consistently more effectively than either alone, reaching maximum inhibition levels 51%. Conclusions: specifically inhibits tumorigenic HBV-transfected contrast general displayed interferon-α. This panel lines may be important resource dissecting mechanism which thymosin, other drugs, influences hepatocytes and/or HBV-associated carcinoma.