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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: A piperazidine derivative of 23-hydroxy betulinic acid induces a mitochondria-derived ROS burst to trigger apoptotic cell death in hepatocellular carcinoma cells

Fig. 1

B5G9 suppresses HepG2 cells in vitro and in vivo. a The cytotoxicity of B5G9 on HepG2 cells. HepG2 cells were treated with different concentrations of B5G9 for 12, 24 and 36 h. Cell viability was measured by MTT assay. b The inhibitory effect of B5G9 on the colony formation of HepG2 cells. HepG2 cells were treated with different concentrations of B5G9 for 24 h. Clonogenic survival of HepG2 cells after B5G9 treatment was measured by the number of clones capable of anchorage-dependent growth. ** P ≤ 0.01 vs control. c The growth curves of HepG2 xenografts. Nude mice bearing HepG2 xenografts were treated with B5G9 (20 or 40 mg/kg/day), 23-HBA (20 mg/kg/day) for 23 days. Tumor size was measured every other day. *** P ≤ 0.001 vs vehicle. d The body weight curves of the mice measured every 2 days. e Tumor weights of HepG2 xenografts dissected after 23 days treatment and the photograph of the tumours isolated from nude mice. * P ≤ 0.05 vs vehicle. f B5G9 had no effect on the spleen index. g-h B5G9 had no significant effect on routine blood indices and serum biochemistrical indices. After 23 days treatment, the mice were killed and blood was collected. Routine blood indices (RBC, WBC, PLT, HGB) and serum biochemistrical indices (CK, AST, ALT and BUN) were measured, ** P ≤ 0.01. i B5G9 had no influence on the function of kidney, spleen, liver and heart. After 23 days treatment, viscera were taken out for H&E staining

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