Fig. 5

β-escin suppresses growth of JIMT-1-derived xenografts. A–D Impact of β-escin on tumor growth. JIMT-1 cells (4×10⁶) were injected into the fourth mammary fat pad of BALB/c nude mice. Animals were intraperitoneally administered with β-escin (4 mg/kg, body weight, 5 times/week for 4 weeks). β-escin administration resulted in a significant decrease in tumor volume (A, **p<0.01, n = 8) and tumor weight (B, ***p<0.001, n = 8). C The tumor burden was markedly reduced in the β-escin-treated group. D No significant alteration in body weight between the β-escin and CTL groups was observed (NS; not significant, n = 8). (E) Representative images of H&E staining in kidney, liver, lung and tumor tissues from the β-escin and CTL groups. The black arrows indicate the apoptotic cells with cell shrinkage and nuclear condensation. F–H Blood biochemical analyses for hepatic and renal function revealed no significant changes in ALT (F), AST (G), and BUN (H) by β-escin administration. ALT, alanine aminotransferase; NS, not significant; AST, aspartate aminotransferase; BUN, blood urea nitrogen. I The effect of β-escin on Ki-67 expression. Sections were immunostained to assess Ki-67 (red) and DAPI (blue) and the percentages of Ki-67-positive cells were quantified (bottom panel, ***p<0.001). J β-escin-induced apoptosis was determined by TUNEL assay. The white arrows indicate the TUNEL-positive apoptotic cells, and the percentages of TUNEL-positive cells were quantified (****p<0.0001). K Tumor angiogenesis was evaluated for each group of xenograft tumors. Tissues were immunostained using an endothelial cell marker CD31 (red) and DAPI (blue). The number of CD31-positive microvessels in the intra-tumoral (****p<0.0001) and peri-tumoral areas (****p<0.0001) were quantified, respectively