Viral Hepatitis
Copyright ©2008 The WJG Press and Baishideng.
World J Gastroenterol. May 14, 2008; 14(18): 2810-2817
Published online May 14, 2008. doi: 10.3748/wjg.14.2810
Figure 2
Figure 2 A: Cytotoxicity of toxin expression plasmids to HepG2 and HepG2. 2.15 cells. β-Gal activities obtained after cotransfection with the β-Gal expressing DNA plasmid p92 (7.5 &mgr;g) and p92 plasmid without insert (7.5 &mgr;g) were set to 100%. Activities resulting from coexpression of toxin plasmids (p77, p95, p100) and β-Gal expressing plasmid p92 are expressed as relative levels. p95, coexpression of p95 with the toxin gene in opposite orientation to the CMV promoter; p100, coexpression of p100 with the active toxin fragment under control of the CMV promoter. Cell viability after cotransfection was determined by β-Gal activity from the β-Gal expressing plasmid. Reduced activity reflects cytotoxicity. B: Cytotoxicity of toxin of sense and antisense RNA. Transfection of PE sense and antisense RNA in HepG2 and HepG2.2.15 cells. RT dependent toxicity of antisense toxin RNA in HepG2 and HepG2.2.15 cells was determined. The β-Gal activities obtained after cotransfection with the β-Gal expressing DNA plasmid p92 (7.5 &mgr;g) and in vitro transcribed r92 control RNA (7.5 &mgr;g) were set to 100%. Activities resulting from coexpression of toxin RNA (r77, r95, r100) and β-Gal expressing plasmid p92 are expressed as relative levels. r77, antisense RNA of inactivated toxin from p77; r95, sense toxin RNA from p95; r100, antisense RNA of active toxin from p100.