| Summary: | Introduction: The aim of this study was to evaluate whether delphinidin is cytoprotective or cytotoxic in osteosarcoma cell lines, and to elucidate the underlying mechanisms. Materials and methods: The present study investigated whether apoptosis or autophagy is induced by delphinidin in human osteosarcoma cell lines. Delphinidin was used as the antioxidant, along with two autophagy inhibitors: 3-methyladenine and bafilomycin A1. Cell viability and known autophagic markers, such as LC3-II expression, were evaluated. Reactive oxygen species (ROS) formation and cell cycle analysis were also investigated. Results: Delphinidin showed concentration-dependent cytotoxicity to osteosarcoma cell. Delphinidin is closely associated with apoptotic cell death mechanisms and pathways related to ROS accumulation. In addition, we observed delphinidin-induced autophagosome formation and increasing levels of LC3-II conversion. However, in spite of delphinidin induced autophagy, the cytotoxic effects induced in the osteosarcoma cells may not be operating via autophagic cell death mechanisms. Conclusions: Delphinidin compromises the cellular protective mechanisms by inhibiting autophagy, permitting ROS to accumulate and finally enhance apoptotic cell death. Our results indicate that delphinidin may play a critical role as a chemotherapeutic agent by preventing the development and progression of osteosarcoma cells. Keywords: Delphinidin, Cytotoxicity, Autophagy, Apoptosis, Osteosarcoma
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