Effects of the tyrosine protein kinase inhibitor genistein on the proliferation, activation of cultured rat hepatic stellate cells

Figure 1 Genistein inhibited the basal and PDGF-BB induced proliferation of HSCs. Cell proliferation was measured by MTT incorporation.

Figure 2 Flow cytometric analysis of cell cycle of HSC. (A) Control HSC; (B) HSCs stimulated with 10 μg·L^-1 PDGF-BB for 15 min; (C) HSC treated with 10^-7 mol/L genistein for 48 h; (D) HSC stimulated with 10 μg·L^-1 PDGF-BB for 15 min and then incubated with 10^-7 mol/L genistein for 48 h.

Figure 3 Immunoflurescence detection of α-SMA in HSC by confocal laser microscopy (× 600). (A) Strong staining was observed in control HSC; (B) only a few cells were stained when HSC treated with 10^-7 mol/L genistein for 48 h.

Figure 4 Flow cytometric analysis of α-SMA in HSC. (A, B) control HSC (C, D) HSC treated with 10^-7 mol/L genistein for 48 h. Showed significant decreased fluorescence intensity (P < 0.05).

Figure 5 Immunoflurescence detection of the expression of tyrosine phosphorylation in HSC by confocal laser microscopy (× 200). (A) HSC stimulated with 10 μg·L^-1 PDGF-BB for 15 min showed a strong staining for phosphoyrosine containing protein; (B) HSCs stimulated with 10 μg·L^-1 PDGF-BB for 15 min and then incubated with 10^-7 mol/L genistein for 48 h showed significant decreased fluorescence intensity for phosphoyrosine containing protein.

Figure 6 Flow cytometric analysis of c-fos (A), c-jun (B) and cyclin D₁ (C) expression in HSC. -indicated the control HSC and -indicated HSC treated with 10^-7 mol/L genistein for 48 h.