Basic Research
Copyright ©2006 Baishideng Publishing Group Co.
World J Gastroenterol. Mar 7, 2006; 12(9): 1379-1385
Published online Mar 7, 2006. doi: 10.3748/wjg.v12.i9.1379
Figure 1
Figure 1 Effects of GLPG on proliferation of L-02 cells treated with GLPG at the concentration of 2-1024 μg/mL for 2 d (A) and at the concentration of 200 μg/mL for 3 d (B). Viable cells were detected every 24 h. The cells untreated with GLPG were used as controls in experiment. Results shown represent the mean ± SD for at least three separate experiments.
Figure 2
Figure 2 Effects of GLPG on ALT and AST activities in CCl4-induced L-02 cell (n =  3) injury. Compared to control group, GLPG suppressed the activities of ALT and AST in the other groups. Results shown represent the mean ± SD from three separate experiments.
Figure 3
Figure 3 Effect of GLPG on SOD activity in serum of rats. The rats were administered orally with or without GLPG at 1000 mg/kg and 3000 mg/kg. The increment of SOD activities was 57.2 % and 70.6 %, respectively.
Figure 4
Figure 4 Histological changes (marked by arrows) of CCl4-induced hepatic injury in the presence or absence of GLPG in mice by hematoxylin-eosin (H&E) staining in control group (A), GLPG group (B), and CCl4-induced liver injury group (C-J) 24 and 72 h after GLPG pretreatment at different doses(0, 300, 600 and 900 mg/kg).
Figure 5
Figure 5 Effect of GLPG on the levels of TNF-ɑ in the plasma of mice, as determined by TNF-ɑ radioimmunoassay kit. Compared with control group, administration of GLPG at various doses could significantly suppress the level of TNF-ɑ in a dose-dependent manner after 48 h. Data are the mean ± SD from 4 determinations.