Effects of c-myb antisense RNA on TGF-β1 and α1-I collagen expression in cultured hepatic stellate cells

Figure 1 Expression of c-myb mRNA, internal control and c-myb protein by RT-PCR, density and Western blot. A: c-myb mRNA expression assayed by semi-quantitative RT-PCR analysis of total RNA. Co-amplification of GAPDH in all samples served as an internal standard. Lane 1: control HSC; Lane 2: pDOR treated HSC; Lane 3: pDOR-myb treated HSC; Lane M: 100 bp ladder. B: Relative expression levels are shown as percent of the internal control by densitometry scanning. The results were expressed as mean ± SE (n = 3). ^bP < 0.01 vs pDOR and control. C: Western-blotting of c-myb protein expression. Fifty µg of extracted cellular protein was loaded in each lane. Lane1: control HSC; Lane2: pDOR treated HSC; Lane3: pDOR-myb treated HSC.

Figure 2 Measurements of cell proliferation with MTT method in three groups of HSCs. The results were expressed as mean ± SE (n = 6). ^bP < 0.01 vs pDOR and control.

Figure 3 Expression of TGF-β1 and α₁-I collagen mRNA. A: α₁-I collagen mRNA expression assayed by semi-quantitative RT-PCR analysis. Lane 1: pDOR-myb treated HSC; Lane 2: control HSC; Lane 3: pDOR treated HSC. B: TGF-β1 mRNA expression assayed by semi-quantitative RT-PCR analysis. Lane 1: pDOR treated HSC; Lane 2: control HSC; Lane 3: pDOR-myb treated HSC. The relative expression levels were shown as percent of the internal control by densitometry scanning. The results were expressed as mean ± SE (n = 3), ^bP < 0.01 vs pDOR and control. Co-amplification of GAPDH in all samples served as an inter-nal standard.