Caspase-dependent mitochondrial apoptotic pathway is involved in astilbin-mediated cytotoxicity in breast carcinoma cells

Astilbin exhibits several pharmacological activities, including hypoglycemic, anti-oxidant and anti-inflammatory properties. The aim of the present study was to investigate the pro-apoptotic activities of astilbin on breast cancer in cells and mice. It was demonstrated that astilbin significantly reduced the cell viability, increased the cell apoptosis rate, suppressed the migration ability, caused the dissipation of the mitochondrial membrane potential and induced the overaccumulation of intracellular reactive oxygen species in MCF-7 and MDA-MB-231 cells after 12 or 24 h of exposure. Data obtained from western blotting suggested that astilbin suppressed the expression levels of B-cell lymphoma 2 (Bcl-2), while it increased the expression levels of cleaved caspase-3, -8 and -9, and Bcl-2-associated X protein in breast carcinoma cells. Furthermore, astilbin inhibited the growth of MCF-7-xenografted tumors in nude mice without influencing their body weights or organ (liver, spleen and kidney) functions. Additionally, astilbin enhanced the expression of pro-apoptotic proteins and suppressed the expression of anti-apoptotic proteins in tumor tissues. All these results revealed that astilbin exhibits pro-apoptotic properties in breast carcinoma cells via modulation of the caspase-dependent pathway, which highlights the feasibility of astilbin as a candidate agent for breast cancer treatment.