Sulforaphane and myricetin act synergistically to induce apoptosis in 3T3-L1 adipocytes

The aim of the present study was to investigate whether sulforaphane (SFN) and myricetin (Myr) synergistically induce apoptosis in adipocytes. The viability of mature 3T3‑L1 adipocytes treated with 40 µM SFN and/or 100 µM Myr was assessed using an MTT assay. Apoptosis was assessed by Hoechst 33258 nuclear staining, and by detection of single‑stranded DNA using an enzyme‑linked immunosorbent assay. Compared with the effects of each compound alone, the combination of SFN and Myr synergistically reduced cell viability, induced apoptosis, increased pro‑apoptotic Bcl‑2 associated X protein expression, decreased anti‑apoptotic B‑cell lymphoma‑2 expression, enhanced Bcl‑2‑associated death promoter (Bad) translocation from the cytoplasm to the mitochondria, and reduced Bad phosphorylation at Ser112. These effects were accompanied by increased cleavage of caspase 3 and poly‑ADP‑ribose‑polymerase. In addition, combined SFN and Myr treatment significantly decreased the protein expression levels of phosphorylated AKT serine/threonine kinase 1 (Akt) at Ser473, as well as the phosphorylation of the downstream protein ribosomal protein, S6 kinase β‑1. Therefore, SFN plus Myr was a more potent inducer of apoptosis in 3T3‑L1 adipocytes than either compound alone. The results of the present study suggest that the mechanism of SNF/Myr‑induced apoptosis involved activation of the Akt‑mediated mitochondrial apoptotic pathway. This may aid treatment of animal models of obesity and preclinical testing.